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ALB — MAPK6

Text-mined interactions from Literome

Hattori et al., Hypertension 2002 (MAP Kinase Signaling System) : In the present study, we show that glycated serum albumin ( GSA ) induces a parallel activation of the redox-responsive transcription factors ( nuclear factor kappaB ) and AP-1 and increases activity of mitogen activated protein kinases ( MAPKs ), extracellular signal regulated kinase ( ERK ), and p38 MAPK in vascular smooth muscle cells ( VSMCs )
Takaya et al., American journal of physiology. Renal physiology 2003 (Cell Transformation, Viral) : In this study, we examined whether albumin overload induced MCP-1 expression was regulated by mitogen activated protein kinase ( MAPK ) in mouse proximal tubular ( mProx ) cells
Murayama et al., J Cell Sci 2004 (Neoplasms) : For the possible mechanism of ALB6 induced apoptosis, ALB6 activated the c-Jun NH2-terminal kinase/stress activated protein kinase ( JNK/SAPK ) and p38 mitogen-activated-protein kinase ( MAPK ) within 5-15 minutes, as well as caspase-3 within 24-48 hours ... It is noteworthy that ALB6 induced tyrosine phosphorylation of the p46 Shc isoform specifically and that the overexpression of its dominant negative form completely suppressed the ALB6 induced activation of JNK/SAPK, p38 MAPK and caspase-3, resulting in the inhibition of apoptotic cell death
Tang et al., J Am Soc Nephrol 2006 (Diabetic Nephropathies...) : Also in a dose dependent manner, GA ( 0.5 mg/ml ) but not albumin caused nuclear translocation of NF-kappaB and activation of mitogen activated protein kinase ( MAPK ) p44/p42 and signal transducer and activator of transcription ( STAT-1 )
Diwakar et al., Biochem Biophys Res Commun 2008 (MAP Kinase Signaling System) : The adaptor phosphoprotein Disabled-2 (Dab2) is known to interact with the cytoplasmic tail of megalin and may be involved in albumin mediated MAPK signalling
Pengal et al., American journal of physiology. Renal physiology 2011 (Disease Models, Animal...) : Serum albumin activated p38 MAPK/MK-2 signaling and induced Cox-2 expression, and these responses were blocked by both inhibitors