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Overexpression of MCPIP1 induced apoptosis.
MCPIP1 is the target of mmu-miR (show MLXIP ELISA Kits)-27-5p.
MCPIP1-MSCs also expressed increased levels of proteins involved in angiogenesis, autophagy, and induction of differentiation
This studies demonstrated that MCPIP1 is an important mediator of minocycline-induced protection from brain ischemia.
Data indicate that MCPIP1 (also termed Regnase-1, encoded by Zc3h12a) knockdown enhanced interleukin-17 (IL-17 (show IL17A ELISA Kits))-mediated signaling.
MCPIP expression in the ischemic myocardium protects against adverse cardiac remodeling and dysfunction following myocardial infarction
both in vivo and in vitro experiments demonstrate that the transcription factors STAT6 (show STAT6 ELISA Kits) and KLF4 (show KLF4 ELISA Kits) implement IL-4 (show IL4 ELISA Kits)-induced M2 polarization via the dual catalytic activities of MCPIP.
Findings reveal that differential regulation of mRNAs by Regnase-1 and Roquin (show RC3H1 ELISA Kits) depends on their translation status and enables elaborate control of inflammation.
Roquin (show RC3H1 ELISA Kits) inhibited T(H)17 cell differentiation and acted together with the endoribonuclease regnase-1 to repress target mRNA encoding the T(H)17 cell-promoting factors IL-6 (show IL6 ELISA Kits), ICOS (show ICOS ELISA Kits), c-Rel (show NFkBP65 ELISA Kits), IRF4 (show IRF4 ELISA Kits), IkappaBNS and IkappaBzeta (show NFKBIZ ELISA Kits).
MCPIP1 deficiency in mice results in severe anemia related to autoimmune mechanisms.
propose that KSHV infection inhibits a negative regulator of miRNA biogenesis (MCPIP1) and up-regulates critical miRNA processing components to evade host mechanisms that inhibit expression of viral miRNAs
both human and cynomolgus monkey MCPIP1 restrict simian immunodeficiency virus replication. Unlike SAMHD1, MCPIP1-mediated HIV-1 restriction cannot be overcome by SIV Vpx.
Regnase-1 can be induced by HMGB1 (show HMGB1 ELISA Kits) in microglia and negatively regulates HMGB1 (show HMGB1 ELISA Kits)-mediated neuroinflammation and neuronal toxicity
findings provide novel insight into the potential targeting of MCPIP1 or autophagy in the development of potential therapeutic strategies for silicosis
These findings reveal a new potential function of MCPIP1, suggesting a possible mechanism of fibrosis in pulmonary silicosis.
The human conserved stem-loop structure is not sufficient for ZC3H12A-dependent degradation.
expression of miR (show MLXIP ELISA Kits)-3613-3p might be regulated by MCPIP1 by cleavage of its precursor form.
Suggest that MCPIP1 may play an important role in cholesterol induced damage in endothelial cells.
Findings show increased MCP1P expression in a model of Ischemia/Reperfusion Injury (I/R) and suggest a vital role for MCPIP1 in cell migration and apoptosis, resulting in increased angiogenesis and apoptosis during the late stages of I/R.
In white blood cells from patients with SLE, MCPIP1 expression was elevated, and its expression correlated positively with the IFN score and negatively with the miR (show MLXIP ELISA Kits)-146a transcript level.
ZC3H12A is an MCP1 (CCL2\; MIM 158105)-induced protein that acts as a transcriptional activator and causes cell death of cardiomyocytes, possibly via induction of genes associated with apoptosis.
zinc finger CCCH-type containing 12A
, MCP-1 treatment-induced protein
, MCP-induced protein 1
, ribonuclease ZC3H12A
, zinc finger CCCH domain-containing protein 12A
, Zinc finger CCCH domain-containing protein 12A
, MCP induced protein 1