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these results indicate that PIAS1 is a positive regulator of MYC (Montrer MYC Kits ELISA).
PIAS1 overexpression exacerbated mutant Huntingtin-associated (Montrer KALRN Kits ELISA) phenotypes and aberrant protein accumulation
Pias1 expression in primary myoblasts enhances the induction of cardiac muscle genes MyoD (Montrer MYOD1 Kits ELISA), Myogenin (Montrer MYOG Kits ELISA) and Myomaker. Endothelial cell specific inactivation of Pias1 in vivo impairs yolk sac (Montrer ADCY10 Kits ELISA) erythrogenesis, angiogenesis and recapitulates loss of myocardium muscle mass. Pias1 is an essential gene for YS erythropoiesis and vasculogenesis in vivo.
Data suggest overexpression of Pias1 in white adipose tissue (WAT) of obesity/prediabetes improves insulin (Montrer INS Kits ELISA) resistance; knockdown of Pias1 in normal WAT leads to insulin (Montrer INS Kits ELISA) resistance; Pias1 expression in WAT is down-regulated by c-Jun N-terminal kinase.
Between the E3 SUMO ligase PIAS1 and STAT-3 (Montrer STAT3 Kits ELISA).
Knockdown of PIAS1 in astrocytes impairs the accumulation of nuclear STI1 (Montrer STIP1 Kits ELISA) in response to irradiation. Moreover, a PIAS1 mutant lacking the STI1 (Montrer STIP1 Kits ELISA) binding site is unable to increase STI1 (Montrer STIP1 Kits ELISA) nuclear retention.
A novel role of PIAS1 in maintaining the quiescence of dormant hematopoietic stem cells and in the epigenetic repression of the myeloerythroid program.
The present study showed that PIAS1 functions as a SUMO E3 ligase of C/EBPbeta (Montrer CEBPB Kits ELISA) to regulate adipogenesis.
Piasy (Montrer PIAS4 Kits ELISA) represses the synergistic activation of PITX2 (Montrer PITX2 Kits ELISA) with interacting co-factors and Piasy (Montrer PIAS4 Kits ELISA) represses Pias1 activation of PITX2 (Montrer PITX2 Kits ELISA) transcriptional activity.
MAPK-activated protein kinase-2 limits endothelial inflammation via the PIAS1 S522 phosphorylation-mediated increase in PIAS1 transrepression and SUMO ligase activity.
PIAS1 is a prognostic biomarker in breast cancer
PIAS1 is a determinant of poor survival and acts as a positive feedback regulator of AR signaling through enhanced AR stabilization in prostate cancer
HBs protein-induced hPIAS1 transcription requires TAL1 (Montrer TAL1 Kits ELISA), E47 (Montrer TCF3 Kits ELISA), MYOG (Montrer MYOG Kits ELISA), NFI (Montrer NFIC Kits ELISA), and MAPK (Montrer MAPK1 Kits ELISA) signal pathways
identified the SUMO ligase PIAS1 as a constituent PML (Montrer PML Kits ELISA)-NB antiviral protein. This finding distinguishes a SUMO ligase that may mediate signaling events important in promyelocytic leukemia (Montrer PML Kits ELISA) nuclear body mediated intrinsic immunity.
PIAS1 enhances p300 (Montrer EP300 Kits ELISA) recruitment to c-Myb (Montrer MYB Kits ELISA)-bound sites through interaction with both proteins. In addition, the E3 activity of PIAS1 enhances further its coactivation
Results show that apocrine breast cancer and prostate cancer cells share a core AR cistrome and target gene signature linked to cancer cell growth, and PIAS1 plays a similar coregulatory role for AR in both cancer cell types.
c-Myc (Montrer MYC Kits ELISA) is targeted to the proteasome for degradation in a SUMOylation-dependent manner, regulated by PIAS1, SENP7 (Montrer SENP7 Kits ELISA) and RNF4 (Montrer RNF4 Kits ELISA)
Data demonstrate that PIAS1 interacts with TRF2 (Montrer TERF2 Kits ELISA) and mediates its sumoylation serving as a molecular switch that controls the level of TRF2 (Montrer TERF2 Kits ELISA) at telomeres.
This gene encodes a member of the mammalian PIAS
protein inhibitor of activated STAT, 1
, DEAD/H (Asp-Glu-Ala-Asp/His) box binding protein 1
, DEAD/H box-binding protein 1
, E3 SUMO-protein ligase PIAS1
, protein inhibitor of activated STAT protein 1
, AR interacting protein
, RNA helicase II-binding protein
, gu-binding protein
, protein inhibitor of activated STAT-1
, zinc finger, MIZ-type containing 3
, SUMO E3 ligase