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PRLR — SOCS3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: PRLR → SOCS3 (decreases, SOCS3 Activity) Dif et al., Endocrinology 2001*
  Evidence: SOCS-2 can play a more important potentiator role on PRL signaling, resulting in a restoration of 50% of transcriptional inhibition induced by SOCS-3 and a restoration of 100% of transcriptional inhibition induced by CIS. SOCS-2 was able to block the inhibitory effect of SOCS-1
• KEGG Jak-STAT signaling pathway: SOCS1/SOCS2/SOCS3/SOCS4/SOCS5/SOCS7 → CNTFR/CRLF2/CSF2RA/CSF2RB/CSF3R/EPOR/GHR/IFNAR1/IFNAR2/IFNGR1/IFNGR2/IFNLR1/IL10RA/IL10RB/IL11RA/IL12RB1/IL12RB2/IL13RA1/IL13RA2/IL15RA/IL20RA/IL20RB/IL21R/IL22RA1/IL22RA2/IL23R/IL2RA/IL2RB/IL2RG/IL3RA/IL4R/IL5RA/IL6R/IL6ST/IL7R/IL9R/LEPR/LIFR/MPL/OSMR/PRLR (protein-protein, inhibition)
  

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: SOCS3 — PRLR (physical association, affinity chromatography technology) Dif et al., Endocrinology 2001*
• IRef Hprd Interaction: SOCS3 — PRLR (in vivo) Dif et al., Endocrinology 2001*
• IRef Ophid Interaction: SOCS3 — PRLR (aggregation, confirmational text mining) Dif et al., Endocrinology 2001*
• IRef Ophid Interaction: SOCS3 — PRLR (aggregation, interologs mapping) Brown et al., Bioinformatics 2005