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Gencode Genes

CTSL3P (ENST00000354530.2) at chr9:87772915-87786884 - Homo sapiens cathepsin L family member 3, pseudogene (CTSL3P), non-coding RNA. (from RefSeq NR_027917)
CTSL (ENST00000343150.10) at chr9:87726119-87731469 - Homo sapiens cathepsin L (CTSL), transcript variant 1, mRNA. (from RefSeq NM_001912)
CTSL (ENST00000495822.1) at chr9:87726134-87731393 - cathepsin L (from HGNC CTSL)
CTSL (ENST00000482054.1) at chr9:87726140-87729680 - cathepsin L (from HGNC CTSL)
CTSL3P (ENST00000412179.5) at chr9:87772453-87774299 - cathepsin L family member 3, pseudogene (from HGNC CTSL3P)
CTSL (ENST00000375894.9) at chr9:87726114-87731073 - cathepsin L (from HGNC CTSL)
CTSL (ENST00000342020.5) at chr9:87726140-87728997 - Belongs to the peptidase C1 family. (from UniProt Q5T8F0)
CTSL (ENST00000340342.10) at chr9:87726109-87731386 - Homo sapiens cathepsin L (CTSL), transcript variant 2, mRNA. (from RefSeq NM_145918)
CTDSPL2 (ENST00000558966.5) at chr15:44427793-44524543 - Probable phosphatase (By similarity). (from UniProt Q05D32)
CTDSPL2 (ENST00000558373.5) at chr15:44459003-44527232 - Probable phosphatase (By similarity). (from UniProt Q05D32)
CTDSPL2 (ENST00000260327.9) at chr15:44427629-44529038 - Homo sapiens CTD small phosphatase like 2 (CTDSPL2), mRNA. (from RefSeq NM_016396)
CTSV (ENST00000538255.5) at chr9:97029679-97039643 - Homo sapiens cathepsin V (CTSV), transcript variant 2, mRNA. (from RefSeq NM_001201575)
CTSV (ENST00000259470.6) at chr9:97029677-97039142 - Homo sapiens cathepsin V (CTSV), transcript variant 1, mRNA. (from RefSeq NM_001333)
PLEKHF1 (ENST00000592810.1) at chr19:29665459-29674843 - May induce apoptosis through the lysosomal-mitochondrial  pathway. Translocates to the lysosome initiating the  permeabilization of lysosomal membrane (LMP) and resulting in the  release of CTSD and CTSL to the cytoplasm. Triggers the caspase-  independent apoptosis by altering mitochondrial membrane  permeabilization (MMP) resulting in the release of PDCD8. (from UniProt Q96S99)
PLEKHF1 (ENST00000436066.4) at chr19:29665461-29675477 - Homo sapiens pleckstrin homology and FYVE domain containing 1 (PLEKHF1), mRNA. (from RefSeq NM_024310)
NSFL1C (ENST00000476071.5) at chr20:1442162-1466918 - Homo sapiens NSFL1 cofactor (NSFL1C), transcript variant 4, mRNA. (from RefSeq NM_001206736)
NSFL1C (ENST00000216879.8) at chr20:1442162-1467692 - Homo sapiens NSFL1 cofactor (NSFL1C), transcript variant 1, mRNA. (from RefSeq NM_016143)
NSFL1C (ENST00000353088.6) at chr20:1442162-1466828 - Homo sapiens NSFL1 cofactor (NSFL1C), transcript variant 2, mRNA. (from RefSeq NM_018839)
CD74 (ENST00000353334.10) at chr5:150401670-150412929 - Homo sapiens CD74 molecule (CD74), transcript variant 2, mRNA. (from RefSeq NM_004355)
CD74 (ENST00000009530.12) at chr5:150400041-150412751 - Homo sapiens CD74 molecule (CD74), transcript variant 1, mRNA. (from RefSeq NM_001025159)
HLA-DQB1 (ENST00000424806.1) at chr6_GL000253v2_alt:4076917-4086211 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt P01920)
HLA-DRB1 (ENST00000328980.11) at chr6_GL000255v2_alt:3779004-3792428 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt Q9GIY3)
HLA-DQA1 (ENST00000444296.6) at chr6_GL000256v2_alt:4039371-4045152 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt P01909)
HLA-DQA1 (ENST00000395363.5) at chr6:32637401-32643652 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt P01909)
HLA-DQA1 (ENST00000374949.2) at chr6:32637420-32643017 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt P01909)
HLA-DRB1 (ENST00000428566.5) at chr6_GL000251v2_alt:4000478-4028652 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt Q9GIY3)
HLA-DRB1 (ENST00000415796.5) at chr6_GL000255v2_alt:3781437-3809621 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt Q9GIY3)
HLA-DQA1 (ENST00000399678.5) at chr6_GL000255v2_alt:3836468-3842664 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt P01909)
HLA-DQA1 (ENST00000399675.5) at chr6_GL000255v2_alt:3836468-3842664 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt P01909)
HLA-DRB1 (ENST00000412634.5) at chr6_GL000256v2_alt:3981401-4012352 - Binds peptides derived from antigens that access the  endocytic route of antigen presenting cells (APC) and presents  them on the cell surface for recognition by the CD4 T-cells. The  peptide binding cleft accommodates peptides of 10-30 residues. The  peptides presented by MHC class II molecules are generated mostly  by degradation of proteins that access the endocytic route, where  they are processed by lysosomal proteases and other hydrolases.  Exogenous antigens that have been endocytosed by the APC are thus  readily available for presentation via MHC II molecules, and for  this reason this antigen presentation pathway is usually referred  to as exogenous. As membrane proteins on their way to degradation  in lysosomes as part of their normal turn-over are also contained  in the endosomal/lysosomal compartments, exogenous antigens must  compete with those derived from endogenous components. Autophagy  is also a source of endogenous peptides, autophagosomes  constitutively fuse with MHC class II loading compartments. In  addition to APCs, other cells of the gastrointestinal tract, such  as epithelial cells, express MHC class II molecules and CD74 and  act as APCs, which is an unusual trait of the GI tract. To produce  a MHC class II molecule that presents an antigen, three MHC class  II molecules (heterodimers of an alpha and a beta chain) associate  with a CD74 trimer in the ER to form a heterononamer. Soon after  the entry of this complex into the endosomal/lysosomal system  where antigen processing occurs, CD74 undergoes a sequential  degradation by various proteases, including CTSS and CTSL, leaving  a small fragment termed CLIP (class-II-associated invariant chain  peptide). The removal of CLIP is facilitated by HLA-DM via direct  binding to the alpha-beta-CLIP complex so that CLIP is released.  HLA-DM stabilizes MHC class II molecules until primary high  affinity antigenic peptides are bound. The MHC II molecule bound  to a peptide is then transported to the cell membrane surface. In  B-cells, the interaction between HLA-DM and MHC class II molecules  is regulated by HLA-DO. Primary dendritic cells (DCs) also to  express HLA-DO. Lysosomal miroenvironment has been implicated in  the regulation of antigen loading into MHC II molecules, increased  acidification produces increased proteolysis and efficient peptide  loading. (from UniProt Q9GIY3)
CD74 (ENST00000377795.7) at chr5:150401637-150412769 - Homo sapiens CD74 molecule (CD74), transcript variant 5, mRNA. (from RefSeq NM_001364084)
TGM3 (ENST00000381458.6) at chr20:2296001-2341079 - Homo sapiens transglutaminase 3 (TGM3), mRNA. (from RefSeq NM_003245)
HLA-DQB2 (ENST00000430849.6) at chr6_GL000252v2_alt:4000854-4008293 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 1, mRNA. (from RefSeq NM_001300790)
HLA-DQB2 (ENST00000457432.6) at chr6_GL000253v2_alt:4175450-4182889 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 1, mRNA. (from RefSeq NM_001300790)
HLA-DQB2 (ENST00000432486.6) at chr6_GL000254v2_alt:4055473-4062912 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 1, mRNA. (from RefSeq NM_001300790)
HLA-DQB2 (ENST00000399661.4) at chr6_GL000255v2_alt:3950399-3957838 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 1, mRNA. (from RefSeq NM_001300790)
HLA-DQB2 (ENST00000456529.1) at chr6_GL000250v2_alt:4062237-4069630 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 2, mRNA. (from RefSeq NM_001198858)
HLA-DQB2 (ENST00000438757.1) at chr6_GL000251v2_alt:4169671-4177064 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 2, mRNA. (from RefSeq NM_001198858)
HLA-DQB2 (ENST00000426733.5) at chr6_GL000256v2_alt:4156243-4163635 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 2, mRNA. (from RefSeq NM_001198858)
HLA-DQB2 (ENST00000411527.5) at chr6:32756098-32763490 - Homo sapiens major histocompatibility complex, class II, DQ beta 2 (HLA-DQB2), transcript variant 2, mRNA. (from RefSeq NM_001198858)
HLA-DQA2 (ENST00000453672.2) at chr6_GL000253v2_alt:4160657-4166218 - Homo sapiens major histocompatibility complex, class II, DQ alpha 2 (HLA-DQA2), mRNA. (from RefSeq NM_020056)
HLA-DQA2 (ENST00000446482.2) at chr6_GL000255v2_alt:3935606-3941465 - Homo sapiens major histocompatibility complex, class II, DQ alpha 2 (HLA-DQA2), mRNA. (from RefSeq NM_020056)
HLA-DQA2 (ENST00000241802.9) at chr6_GL000254v2_alt:4040716-4046584 - Homo sapiens major histocompatibility complex, class II, DQ alpha 2 (HLA-DQA2), mRNA. (from RefSeq NM_020056)
HLA-DQA2 (ENST00000415898.2) at chr6_GL000256v2_alt:4141489-4147359 - Homo sapiens major histocompatibility complex, class II, DQ alpha 2 (HLA-DQA2), mRNA. (from RefSeq NM_020056)
HLA-DRA (ENST00000383127.6) at chr6_GL000251v2_alt:3877968-3883135 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRA (ENST00000416883.6) at chr6_GL000252v2_alt:3680147-3685357 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRA (ENST00000442960.6) at chr6_GL000253v2_alt:3744059-3749270 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRA (ENST00000414698.6) at chr6_GL000254v2_alt:3780808-3786018 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRA (ENST00000383259.6) at chr6_GL000255v2_alt:3662891-3668101 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRA (ENST00000411524.6) at chr6_GL000256v2_alt:3754985-3760195 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRA (ENST00000395388.7) at chr6:32439887-32445046 - Homo sapiens major histocompatibility complex, class II, DR alpha (HLA-DRA), mRNA. (from RefSeq NM_019111)
HLA-DRB1 (ENST00000444645.6) at chr6_GL000252v2_alt:3814543-3830112 - Homo sapiens major histocompatibility complex, class II, DR beta 1 (HLA-DRB1), transcript variant 3, mRNA. (from RefSeq NM_001359193)
HLA-DRB1 (ENST00000437784.6) at chr6_GL000253v2_alt:3988943-4004557 - Homo sapiens major histocompatibility complex, class II, DR beta 1 (HLA-DRB1), transcript variant 3, mRNA. (from RefSeq NM_001359193)
HLA-DRB4 (ENST00000411565.2) at chr6_GL000256v2_alt:3851133-3866096 - Homo sapiens major histocompatibility complex, class II, DR beta 4 (HLA-DRB4), mRNA. (from RefSeq NM_021983)
HLA-DQA1 (ENST00000418023.5) at chr6_GL000256v2_alt:4039288-4045152 - Homo sapiens major histocompatibility complex, class II, DQ alpha 1 (HLA-DQA1), mRNA. (from RefSeq NM_002122)
HLA-DQA1 (ENST00000383251.6) at chr6_GL000255v2_alt:3836385-3842664 - Homo sapiens major histocompatibility complex, class II, DQ alpha 1 (HLA-DQA1), mRNA. (from RefSeq NM_002122)
HLA-DQA1 (ENST00000343139.10) at chr6:32637406-32643671 - Homo sapiens major histocompatibility complex, class II, DQ alpha 1 (HLA-DQA1), mRNA. (from RefSeq NM_002122)
HLA-DQB1 (ENST00000419914.6) at chr6_GL000253v2_alt:4076917-4084516 - Homo sapiens major histocompatibility complex, class II, DQ beta 1 (HLA-DQB1), transcript variant 3, mRNA. (from RefSeq NM_001243962)
HLA-DRB5 (ENST00000374975.4) at chr6:32517353-32530287 - Homo sapiens major histocompatibility complex, class II, DR beta 5 (HLA-DRB5), mRNA. (from RefSeq NM_002125)
HLA-DRB3 (ENST00000383126.7) at chr6_GL000251v2_alt:3934009-3947126 - Homo sapiens major histocompatibility complex, class II, DR beta 3 (HLA-DRB3), mRNA. (from RefSeq NM_022555)
HLA-DRB3 (ENST00000307137.11) at chr6_GL000255v2_alt:3715358-3728445 - Homo sapiens major histocompatibility complex, class II, DR beta 3 (HLA-DRB3), mRNA. (from RefSeq NM_022555)
HLA-DRB1 (ENST00000399450.6) at chr6_GL000251v2_alt:3998045-4011459 - Homo sapiens major histocompatibility complex, class II, DR beta 1 (HLA-DRB1), transcript variant 2, mRNA. (from RefSeq NM_001243965)
HLA-DRB1 (ENST00000419393.6) at chr6_GL000256v2_alt:3979128-3993834 - Homo sapiens major histocompatibility complex, class II, DR beta 1 (HLA-DRB1), transcript variant 4, mRNA. (from RefSeq NM_001359194)
HLA-DPB1 (ENST00000454006.6) at chr6_GL000252v2_alt:4319457-4330724 - Homo sapiens major histocompatibility complex, class II, DP beta 1 (HLA-DPB1), mRNA. (from RefSeq NM_002121)
HLA-DPB1 (ENST00000399500.6) at chr6_GL000255v2_alt:4270558-4281835 - Homo sapiens major histocompatibility complex, class II, DP beta 1 (HLA-DPB1), mRNA. (from RefSeq NM_002121)
HLA-DPB1 (ENST00000433800.6) at chr6_GL000256v2_alt:4524909-4536184 - Homo sapiens major histocompatibility complex, class II, DP beta 1 (HLA-DPB1), mRNA. (from RefSeq NM_002121)
HLA-DPB1 (ENST00000418931.7) at chr6:33075990-33089696 - Homo sapiens major histocompatibility complex, class II, DP beta 1 (HLA-DPB1), mRNA. (from RefSeq NM_002121)
CTSLP8 (ENST00000413075.2) at chr9:87844154-87847314 - cathepsin L pseudogene 8 (from HGNC CTSLP8)
CTSLP3 (ENST00000628708.1) at chr10:46753605-46758198 - cathepsin L pseudogene 3 (from HGNC CTSLP3)
CTSLP2 (ENST00000580501.2) at chr10:47581211-47582321 - cathepsin L pseudogene 2 (from HGNC CTSLP2)
CTSLP6 (ENST00000458273.2) at chr10:79870375-79873903 - cathepsin L pseudogene 6 (from HGNC CTSLP6)
CTSLP1 (ENST00000457530.1) at chr10:87386685-87390203 - cathepsin L pseudogene 1 (from HGNC CTSLP1)
CTSLP4 (ENST00000454614.1) at chr10:50705380-50708906 - cathepsin L pseudogene 4 (from HGNC CTSLP4)
CTSLP3 (ENST00000629029.1) at chr10:46758089-46759199 - cathepsin L pseudogene 3 (from HGNC CTSLP3)
CTSLP3 (ENST00000626319.2) at chr10:46756991-46759740 - Homo sapiens cathepsin L pseudogene 2 (CTSLP2), non-coding RNA. (from RefSeq NR_033407)

NCBI RefSeq genes, curated subset (NM_*, NR_*, NP_* or YP_*)

NM_001257972.1 at chr9:87726059-87731469
NM_001257973.1 at chr9:87726059-87731469
NM_145918.2 at chr9:87726059-87731469
NM_001257971.1 at chr9:87726059-87731469
NM_001912.4 at chr9:87726059-87731469
NR_027917.1 at chr9:87772915-87786884
NR_033407.1 at chr10:47580671-47583419
NR_033405.1 at chr9:87844745-87847424

NCBI RefSeq genes, predicted subset (XM_* or XR_*)

XM_017014293.2 at chr9:87725437-87731387
XM_011518263.1 at chr9:87725519-87731393
XM_005251716.4 at chr9:87726086-87731393

NCBI RefSeq and Ensembl transcripts from the MANE Project (v0.6)

CTSL at chr9:87726119-87731469

RefSeq Genes

CTSL at chr9:87726119-87731469 - (NM_001257971) cathepsin L1 isoform 1 preproprotein
CTSL at chr9:87726119-87731469 - (NM_001257973) cathepsin L1 isoform 2
CTSL at chr9:87726119-87731469 - (NM_001257972) cathepsin L1 isoform 1 preproprotein
CTSL at chr9:87726119-87731469 - (NM_145918) cathepsin L1 isoform 1 preproprotein
CTSL at chr9:87726119-87731469 - (NM_001912) cathepsin L1 isoform 1 preproprotein
CTSL3P at chr9:87772915-87786884 - (NR_027917) 
CTSLP2 at chr10:47580671-47583419 - (NR_033407) 
CTSLP8 at chr9:87844745-87847424 - (NR_033405) 

NCBI RefSeq other annotations (not NM_*, NR_*, XM_*, XR_*, NP_* or YP_*)

CTSLP6 at chr10:79870051-79873915
CTSLP4 at chr10:50704658-50708915
CTSLP3 at chr10:46758089-46759065
CTSLP1 at chr10:87386361-87390215

Non-Human RefSeq Genes

ctsl at chr9:97032958-97037395 - (NM_001292876) cathepsin L1 precursor
ctsl at chr9:87728030-87847310 - (NM_001310011) cathepsin L1 precursor
ctsl at chr9:87728025-87731107 - (NM_001200253) cathepsin L1 precursor
ctsl at chr9:97032949-97037398 - (NM_001104686) cathepsin L1 precursor
CTSL at chr9:97032807-97038055 - (NM_001083686) cathepsin L1 precursor
CTSL at chr9:87727593-87731305 - (NM_001083686) cathepsin L1 precursor
CTSL at chr10:87386685-87390212 - (NM_001083686) cathepsin L1 precursor
CTSL at chr10:79870253-79873912 - (NM_001083686) cathepsin L1 precursor
Ctsl at chr9:87728025-87847318 - (NM_013156) cathepsin L1 preproprotein
Ctsl at chr9:97032877-97038051 - (NM_013156) cathepsin L1 preproprotein
Ctsl at chr9:97032813-97038051 - (NM_009984) cathepsin L1 preproprotein
ctsl.1 at chr9:97032949-97036747 - (NM_001002368) cathepsin L.1 precursor
ctsl.1 at chr9:87728582-87730448 - (NM_001002368) cathepsin L.1 precursor
ctsla at chr10:87386685-87389452 - (NM_212584) cathepsin L1 precursor
ctsla at chr10:50705380-50707936 - (NM_212584) cathepsin L1 precursor
ctslb at chr9:87728582-87730448 - (NM_131198) cathepsin Lb precursor
ctsll at chr9:87728030-87846691 - (NM_001005999) cathepsin L, like
Ctsll3 at chr9:87728310-87847330 - (NM_027344) cathepsin L-like 3 precursor

Basic Gene Annotation Set from GENCODE Version 31 (Ensembl 97)

CTSL at chr9:87726109-87731386
CTSL at chr9:87726119-87731469
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 31 (Ensembl 97)

CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726119-87731469
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 29 (Ensembl 94)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 29 (Ensembl 94)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 28 (Ensembl 92)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 28 (Ensembl 92)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 27 (Ensembl 90)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 27 (Ensembl 90)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 26 (Ensembl 88)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 26 (Ensembl 88)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 25 (Ensembl 85)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 25 (Ensembl 85)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 24 (Ensembl 83)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 24 (Ensembl 83)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 23 (Ensembl 81)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 23 (Ensembl 81)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 22 (Ensembl 79)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 22 (Ensembl 79)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

Basic Gene Annotation Set from GENCODE Version 20 (Ensembl 76)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726140-87728997

Comprehensive Gene Annotation Set from GENCODE Version 20 (Ensembl 76)

CTSL at chr9:87725519-87731392
CTSL at chr9:87726109-87731386
CTSL at chr9:87726114-87731073
CTSL at chr9:87726134-87731393
CTSL at chr9:87726140-87728997
CTSL at chr9:87726140-87729680

International Knockout Mouse Consortium Genes Mapped to Human Genome

Ctsll3_46432 at chr9:87844745-87847424
Ctsl_24500 at chr9:87726059-87731469
Ctsl_49838 at chr9:87726059-87731469
Ctsl_70126 at chr9:87726059-87731469

Human Aligned mRNA Search Results

BC023504 - Homo sapiens cathepsin L2, mRNA (cDNA clone MGC:2011 IMAGE:3139314), complete cds.
CR457053 - Homo sapiens full open reading frame cDNA clone RZPDo834B0418D for gene CTSL, cathepsin L; complete cds, incl. stopcodon.
BC110512 - Homo sapiens cathepsin L2, mRNA (cDNA clone MGC:125957 IMAGE:40031744), complete cds.
BC012612 - Homo sapiens cathepsin L1, mRNA (cDNA clone MGC:13635 IMAGE:4295635), complete cds.
BC142983 - Homo sapiens cathepsin L1, mRNA (cDNA clone MGC:167089 IMAGE:8860422), complete cds.
L25629 - Human cathepsin-L-like (CTSLL3) mRNA.
L25628 - Human cathepsin-L-like (CTSLL2) mRNA.
AK312806 - Homo sapiens cDNA, FLJ93235, highly similar to Homo sapiens cathepsin L2 (CTSL2), mRNA.

Human Unaligned mRNA Search Results

NR_033405 - Homo sapiens cathepsin L pseudogene 8 (CTSLP8), non-coding RNA.
NR_033407 - Homo sapiens cathepsin L pseudogene 2 (CTSLP2), non-coding RNA.
NR_027917 - Homo sapiens cathepsin L family member 3, pseudogene (CTSL3P), non-coding RNA.

Non-Human Aligned mRNA Search Results

BC134741 - Bos taurus cathepsin L1, mRNA (cDNA clone MGC:157400 IMAGE:8387836), complete cds.
BC102312 - Bos taurus cathepsin L2, mRNA (cDNA clone MGC:127464 IMAGE:7949185), complete cds.
BC108031 - Danio rerio cathepsin L, 1 b, mRNA (cDNA clone MGC:123162 IMAGE:7284757), complete cds.
BC083200 - Danio rerio cathepsin L, like, mRNA (cDNA clone MGC:101557 IMAGE:7222106), complete cds.
BC075887 - Danio rerio cathepsin L.1, mRNA (cDNA clone MGC:92089 IMAGE:7047077), complete cds.
BC066490 - Danio rerio cathepsin L1, a, mRNA (cDNA clone MGC:76945 IMAGE:6525005), complete cds.
CR760760 - Xenopus tropicalis finished cDNA, clone TTpA002p12.
AB099890 - Oryzias latipes ctsL mRNA for cathepsin L, complete cds.
EF015467 - Hippoglossus hippoglossus cathepsin L (ctsL) mRNA, complete cds.
BC068163 - Mus musculus cathepsin L, mRNA (cDNA clone MGC:93008 IMAGE:30359160), complete cds.
BC063175 - Rattus norvegicus cathepsin L1, mRNA (cDNA clone MGC:72924 IMAGE:6918389), complete cds.
LN715177 - Strongyloides stercoralis partial mRNA for Cathepsin L (CtsL gene).
KJ871613 - Marsupenaeus japonicus cathepsin L (CTSL) mRNA, complete cds.
AY890446 - Synthetic construct Homo sapiens clone FLH140202.01X cathepsin L (CTSL) mRNA, complete cds.
AY893779 - Synthetic construct Homo sapiens clone FLH053856.01L cathepsin L (CTSL) mRNA, partial cds.
JT417657 - TSA: Ictalurus punctatus aby_k73:586857 mRNA sequence.
AB128161 - Cyprinus carpio CTSL mRNA for cathepsin L preproprotein, complete cds.
KM522787 - Sparus aurata cathepsin L (CTSL) mRNA, complete cds.
KP455635 - Ctenopharyngodon idella cathepsin L precursor (CTSL) mRNA, complete cds.
MH580287 - Acipenser sinensis cathepsin L (CTSL) mRNA, complete cds.
HG710127 - Tityus serrulatus partial mRNA for cathepsin L-like cysteine peptidase 8 (ctsl gene).
HG710129 - Tityus serrulatus partial mRNA for cathepsin L-like cysteine peptidase 10 (ctsl gene).
HG710154 - Tityus serrulatus partial mRNA for cathepsin L-like cysteine peptidase 1 (ctsl gene).
HG710155 - Tityus serrulatus mRNA for cathepsin L-like cysteine peptidase 2 (ctsl gene).
HG710156 - Tityus serrulatus mRNA for cathepsin L-like cysteine peptidase 3 (ctsl gene).
HG710158 - Tityus serrulatus mRNA for cathepsin L-like cysteine peptidase 5 (ctsl gene).
HG710159 - Tityus serrulatus mRNA for cathepsin L-like cysteine peptidase 6 (ctsl gene).
KT780367 - Ictalurus punctatus cathepsin La (ctsla) mRNA, complete cds.
KX013127 - Tyto alba isolate M022138 cathepsin L2 (CTSL2) mRNA, complete cds.
DQ152935 - Ovis aries cathepsin L2 (CTSL2) mRNA, partial cds.
BC151425 - Bos taurus cathepsin L2, mRNA (cDNA clone MGC:179266 IMAGE:7954194), complete cds.
BT021022 - Bos taurus cathepsin L2 (CTSL2), mRNA, complete cds.
JU323374 - TSA: Macaca mulatta Mamu_506758 mRNA sequence.
JV044398 - TSA: Macaca mulatta Mamu_416601 mRNA sequence.
KX013126 - Tyto alba isolate M022138 cathepsin L1 (CTSL1) mRNA, complete cds.
JU323190 - TSA: Macaca mulatta Mamu_531918 mRNA sequence.
JU471611 - TSA: Macaca mulatta Mamu_369811 mRNA sequence.
JV043388 - TSA: Macaca mulatta Mamu_405325 mRNA sequence.
HG710130 - Tityus serrulatus partial mRNA for cathepsin L-like cysteine peptidase 11 (ctsl gene).