Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.31 (AMP-activated protein kinase)
 13,065 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Par-1 protein kinases are conserved from yeast to man and belong to a subfamily of kinases that includes the energy sensor and metabolic regulator, AMPK. Par-1 is regulated by LKB1 and atypical PKC and has been shown in multiple organisms and cell types to be critical for regulation of cellular polarity. Recent studies using knockout mice have revealed several surprising physiological functions for Par-1b/MARK2/EMK1. Our recent study shows that Par-1b regulates metabolic rate, adiposity and insulin sensitivity. This is the first study to implicate these kinases in metabolic functions akin to those previously defined for AMPK. Conversely, another series of recent publications now implicate AMPK in regulation of polarity. Here we discuss the metabolic phenotype seen in Par-1b deficient mice and the synthesis of several findings that link Par-1 and AMPK to a degree that has not been previously appreciated.
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PMID:The Par-1/MARK family of protein kinases: from polarity to metabolism. 1772 Oct 78

The classical role of AMP-activated protein kinase (AMPK) as an energy status sensor is expanding to include other members of the AMPK family. Recent genetic and cell biological evidence points to a role for MAP/microtubule affinity-regulating kinase 2 (MARK2/EMK/Par1b) in the regulation of metabolic events as well as in the control of CREB-dependent transcription activated by glucose in pancreatic islet beta cells. We have recently developed an in vitro kinase screening platform to identify novel kinase:substrate pairs, the building blocks of signal transduction pathways. Application of this technology led us to identify MARK2 as the kinase that targets a novel glucose-regulated phosphorylation site on Transducer of Regulated CREB Activity 2 (TORC2, referred to as CREB-Regulated Transcriptional Coactivator 2, or CRTC2), a transcriptional coactivator essential for CREB activity in beta cells. We discuss these recent developments and suggest a model whereby members of the AMPK family integrate numerous signals to coordinate energy metabolism and cellular polarity with gene expression to regulate cell function/proliferation.
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PMID:Using kinomics to delineate signaling pathways: control of CRTC2/TORC2 by the AMPK family. 1909 22