Gene interactions and pathways from curated databases and text-mining

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KMT2D — WDR5

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Zhang et al., Endocrine 2004 (MAP Kinase Signaling System) : Moreover, inhibition of a specific mitogen activated protein kinase ( MAPK ) /extracellular signal regulated kinase kinase ( MEK ) by PD98059 blocked FGF2 regulated MEPE/OF45 expressions, indicating that this regulation requires the MAPK pathway ... Moreover, inhibition of a specific mitogen activated protein kinase ( MAPK ) /extracellular signal regulated kinase kinase ( MEK ) by PD98059 blocked FGF2 regulated MEPE/OF45 expressions, indicating that this regulation requires the MAPK pathway
Morales et al., Mol Cell Biol 2005 : We showed previously that MSL3 is essential for the activation of MOF 's nucleosomal histone acetyltransferase activity within an MSL1-MOF complex ... Interaction with MSL1 mediates the activation of MOF in vitro and the targeting of MSL3 to the X-chromosomal territory in vivo
Zhou et al., Zhongguo Wei Zhong Bing Ji Jiu Yi Xue 2005 (Disease Models, Animal...) : Cytokines are the direct mediators for multiple organ failure (MOF), and MOF is triggered by TNF-alpha and a cascade of cytokine release, with a prolonged high-expression of IL-6
Houk et al., Nano Lett 2009 : Importantly, we show conclusively that very rapid TEM induced MOF degradation leads to agglomeration and stable, easily imaged particles, explaining prior reports of particles larger than MOF pores
Liu et al., Nucleic Acids Res 2009 : Over expressing wild-type MEPE/OF45 , but not the mutant MEPE/OF45 ( depleted the key domain to interact with CHK1 ) increases CHK1 levels in the cells and increases the resistance of the cells to IR or CPT. MEPE/OF45, interacting with CHK1, increases CHK1 half-life and decreases CHK1 degradation through the ubiquitine mediated pathway
Li et al., Mol Cell 2009 : We further demonstrate that MOF-MSL1v1 is specifically required for optimal transcription activation of p53 target genes both in vitro and in vivo
Raja et al., Mol Cell 2010 : However, depletion of MCRS2 affects MOF recruitment to promoters
Krishnan et al., Proc Natl Acad Sci U S A 2011 (Aging, Premature...) : Given the reversible nature of epigenetic changes, rescue experiments performed either by Mof overexpression or by histone deacetylase inhibition promoted repair protein recruitment to DNA damage sites and substantially ameliorated aging associated phenotypes, both in vitro and in vivo
Zhang et al., Nucleic Acids Res 2012 : Consistently, enzymatic assays reveal that WDR5 plays an important role in the optimal stimulation of MLL2-4 , SET1A and SET1B methyltransferase activity by the RbBP5-ASH2L heterodimer
Li et al., Cell stem cell 2012 : Mof is also required for Wdr5 recruitment and H3K4 methylation at key regulatory loci, highlighting the complexity and interconnectivity of various chromatin regulators in ESCs
Nath et al., Clin Exp Immunol 1984 (Leprosy) : Non-adherent cell supernatants and MoF from tuberculoid and healthy individuals had little effect on IL-2 production
Shimada et al., Nihon Geka Gakkai Zasshi 1998 (Multiple Organ Failure) : On the other hand, if the antiinflammatory response is greater than the inflammatory response ( CARS ) a compromised state and refractory infection are seen, followed by progressive, irreversible organ dysfunction ( MODS or MOF induced by CARS )