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Suppressed Th17 levels correlated with upregulated expression of negative regulatory genes, PIAS3, SHP2, and SOCS3 in CD4 T cells during acute SIV infection.
Data indicate that PIAS3 (protein inhibitor of activated STAT3) interaction modulates EKLF (erythroid Kruppel-like factor (Montrer KLF1 Kits ELISA)) activity in a promoter-dependent and SUMO-independent manner.
PIAS3 suppresses acute graft-versus-host disease by modulating effector T and B cell subsets through inhibition of STAT3 (Montrer STAT3 Kits ELISA) activation.
These data indicate that tachypacing decreased ATBF1 (Montrer ZFHX3 Kits ELISA), leading to enhanced STAT3 (Montrer STAT3 Kits ELISA) DNA-binding activity due to the reduced formation of a binary complex of ATBF1 (Montrer ZFHX3 Kits ELISA) and PIAS3.
MRL/lpr (Montrer FAS Kits ELISA) mice have significantly increased expressions of STAT3 (Montrer STAT3 Kits ELISA) mRNA and protein and decreased expression of mRNA PIAS3 in the kidneys compared with BALB/C mice.
L97A, R99N and R99Q mutations of the PINIT domain (PIAS3(85-272) ) were found to abrogate binding to STAT3 (Montrer STAT3 Kits ELISA), suggesting that these residues were part of a potential binding surface.
Our results indicate that Pias3-dependent SUMOylation of photoreceptor-specific transcription factors is a common mechanism that controls both rod and cone photoreceptor subtype specification, regulating distinct molecular targets in the two cell types
there is an interaction between Zimp7 (Montrer ZMIZ2 Kits ELISA) and PIAS (Montrer PIAS1 Kits ELISA) proteins with higher preference for PIAS3, in androgen receptor (Montrer AR Kits ELISA)-mediated transcription
results indicate a potential role of PIAS3 as transcriptional modulator of TIF2 (Montrer NCOA2 Kits ELISA)-mediated signalling
role in inducing SUMO-1 (Montrer SUMO1 Kits ELISA) modification and transcriptional repression of IRF-1 (Montrer IRF1 Kits ELISA)
identified a novel conserved domain of 180 residues in PIAS (Montrer PIAS1 Kits ELISA) proteins and showed that its 'PINIT' motif as well as other conserved motifs (in the SAP (Montrer APCS Kits ELISA) box and in the RING domain) are independently involved in nuclear retention of PIAS3L
PAI-1 (Montrer SERPINE1 Kits ELISA) interacted with PIAS3 to regulate Stat3 (Montrer STAT3 Kits ELISA)-dependent gene expression and miR (Montrer MLXIP Kits ELISA)-34a was transcriptionally suppressed by Stat3 (Montrer STAT3 Kits ELISA) to form a positive regulatory loop through Stat3 (Montrer STAT3 Kits ELISA) signaling in non-small cell lung cancer cells.
Levels of PIAS3 are significantly lower, in contrast with phosphorylation of STAT3 (Montrer STAT3 Kits ELISA), in women with endometriosis compared to women without endometriosis.
TRIM8 (Montrer TRIM8 Kits ELISA) activates STAT3 (Montrer STAT3 Kits ELISA) by suppressing the expression of PIAS3, an inhibitor of STAT3 (Montrer STAT3 Kits ELISA), most likely through E3-mediated ubiquitination and proteasomal degradation.
Low PIAS3 expression is associated with breast cancer organoid invasiveness.
SHP2 (Montrer PTPN11 Kits ELISA), SOCS3 (Montrer SOCS3 Kits ELISA) and PIAS3 levels are reduced in medulloblastomas in vivo and in vitro, of which PIAS3 downregulation is more reversely correlated with STAT3 (Montrer STAT3 Kits ELISA) activation. In resveratrol-suppressed medulloblastoma cells with STAT3 (Montrer STAT3 Kits ELISA) downregulation and decreased incidence of STAT3 (Montrer STAT3 Kits ELISA) nuclear translocation, PIAS3 is upregulated, the SHP2 (Montrer PTPN11 Kits ELISA) level remains unchanged and SOCS3 (Montrer SOCS3 Kits ELISA) is downregulated.
The results revealed that although the expression levels of SOCS1 (Montrer SOCS1 Kits ELISA), SOCS3 (Montrer SOCS3 Kits ELISA) and, in particular, pSHP2, tend to decrease in the four types of astrocytomas, PIAS3 downregulation is more negatively correlated with STAT3 (Montrer STAT3 Kits ELISA) activation in the stepwise progress of astrocytomas and would indicate an unfavorable outcome.
3-Formylchromone inhibits proliferation and induces apoptosis of multiple myeloma cells by abrogating STAT3 (Montrer STAT3 Kits ELISA) signaling through the induction of PIAS3.
PIAS3 may serve as a biomarker for predicting hormone therapy stratification, although it is limited to those breast cancer patients receiving hormone therapy.
Taken together, these results suggest that PIAS3 functions as a positive regulator of HIF-1alpha (Montrer HIF1A Kits ELISA)-mediated transcription by increasing its protein stability.
PIAS3 suppression may be protective against joint destruction in rheumatoid arthritis by regulating synoviocyte migration, invasion, and activation.
This gene encodes a member of the PIAS
protein inhibitor of activated STAT, 3
, E3 SUMO-protein ligase PIAS3-like
, e3 SUMO-protein ligase PIAS3-like
, E3 SUMO-protein ligase PIAS3
, protein inhibitor of activated STAT protein 3
, zinc finger, MIZ-type containing 5
, potassium channel regulatory protein KChAP
, potassium channel-associated protein