From top to bottom – research database, the university of dundee brain anoxia

Abstract = oxygen deprivation (hypoxia) triggers a complex network of signaling pathways that result in changed gene expression patterns in order to cope with this challenge. Recent work has identified the serine/threonine kinase HIPK2 as a novel regulatory protein participating in hypoxic gene regulation. HIPK2 can affect apical as well as downstream events during the hypoxic response. Under normoxic conditions, HIPK2-mediated phosphorylation of the ubiquitin E3 ligase siah2 weakens mutual binding and destabilizes the phosphorylated E3 ligase. Low oxygen levels result in strongly increased HIPK2/siah2 interactions that lead to efficient polyubiquitylation and proteasomal degradation of the kinase.Brain anoxia


at the apical level, the siah2 inhibiting phosphorylations are lost, thus allowing siah2-dependent proteolysis of dioxygenases which in turn allows for activation of transcription factor HIF. Downstream events of the hypoxic response are affected by the proteasomal elimination of HIPK2 from gene repressing complexes, an event that allows for full induction of gene expression. Thus HIPK2 can regulate a subset of HIF-dependent and -independent genes during the hypoxic response.,

TY – JOUR

T1 – from top to bottom

T2 – cell cycle

AU – calzado,marco A

AU – de la vega,laureano

AU – munoz,eduardo

AU – schmitz,M. Lienhard

PY – 2009

Y1 – 2009

N2 – oxygen deprivation (hypoxia) triggers a complex network of signaling pathways that result in changed gene expression patterns in order to cope with this challenge.Brain anoxia recent work has identified the serine/threonine kinase HIPK2 as a novel regulatory protein participating in hypoxic gene regulation. HIPK2 can affect apical as well as downstream events during the hypoxic response. Under normoxic conditions, HIPK2-mediated phosphorylation of the ubiquitin E3 ligase siah2 weakens mutual binding and destabilizes the phosphorylated E3 ligase. Low oxygen levels result in strongly increased HIPK2/siah2 interactions that lead to efficient polyubiquitylation and proteasomal degradation of the kinase. At the apical level, the siah2 inhibiting phosphorylations are lost, thus allowing siah2-dependent proteolysis of dioxygenases which in turn allows for activation of transcription factor HIF.Brain anoxia downstream events of the hypoxic response are affected by the proteasomal elimination of HIPK2 from gene repressing complexes, an event that allows for full induction of gene expression. Thus HIPK2 can regulate a subset of HIF-dependent and -independent genes during the hypoxic response.

AB – oxygen deprivation (hypoxia) triggers a complex network of signaling pathways that result in changed gene expression patterns in order to cope with this challenge. Recent work has identified the serine/threonine kinase HIPK2 as a novel regulatory protein participating in hypoxic gene regulation. HIPK2 can affect apical as well as downstream events during the hypoxic response. Under normoxic conditions, HIPK2-mediated phosphorylation of the ubiquitin E3 ligase siah2 weakens mutual binding and destabilizes the phosphorylated E3 ligase.Brain anoxia low oxygen levels result in strongly increased HIPK2/siah2 interactions that lead to efficient polyubiquitylation and proteasomal degradation of the kinase. At the apical level, the siah2 inhibiting phosphorylations are lost, thus allowing siah2-dependent proteolysis of dioxygenases which in turn allows for activation of transcription factor HIF. Downstream events of the hypoxic response are affected by the proteasomal elimination of HIPK2 from gene repressing complexes, an event that allows for full induction of gene expression. Thus HIPK2 can regulate a subset of HIF-dependent and -independent genes during the hypoxic response.

KW – anoxia

KW – apoptosis

KW – carrier proteins

KW – gene expression regulation

brain anoxia

KW – humans

KW – hypoxia-inducible factor 1

KW – nuclear proteins

KW – phosphorylation

KW – protein binding

KW – protein-serine-threonine kinases

KW – signal transduction

KW – ubiquitin-protein ligases

KW – ubiquitination

U2 – 10.4161/cc.8.11.8597

DO – 10.4161/cc.8.11.8597

M3 – article

VL – 8

SP – 1659

EP – 1664

JO – cell cycle

JF – cell cycle

SN – 1538-4101

IS – 11

ER –