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MCPIP1 is a potent negative regulator of psoriatic skin inflammation through IL-17A (show IL17A Proteins) and IL-17C (show IL17C Proteins)
IL-17A (show IL17A Proteins)-mediated induction of MCPIP1 is involved in the regulation of local altered gene expression in suprabasal epidermal layers in psoriasis
Overexpression of MCPIP1 induced apoptosis.
MCPIP1 is the target of mmu-miR (show MLXIP Proteins)-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 Proteins))-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 Proteins) and KLF4 (show KLF4 Proteins) implement IL-4 (show IL4 Proteins)-induced M2 polarization via the dual catalytic activities of MCPIP.
Findings reveal that differential regulation of mRNAs by Regnase-1 and Roquin (show RC3H1 Proteins) depends on their translation status and enables elaborate control of inflammation.
MCPIP1 recognizes regions of the 3'UTR of C/EBPbeta (show CEBPB Proteins) mRNA.
SAHA-mediated suppression of the IL-6 (show IL6 Proteins) expression is achieved through increased recruitment of CEBPalpha to the MCPIP1 promoter and by relieving the miR (show MLXIP Proteins)-9-mediated inhibition of MCPIP1 expression in OA chondrocytes.
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 Proteins) in microglia and negatively regulates HMGB1 (show HMGB1 Proteins)-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.
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