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The protein encoded by MAF is a DNA-binding, leucine zipper-containing transcription factor that acts as a homodimer or as a heterodimer.
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results suggest that pathobiont-dependent inflammatory bowel disease is driven by microbiota-reactive T cells that have escaped this c-MAF-dependent mechanism of iTreg-TH17 homeostasis
c-Maf is a critical transcription factor regulating T-cell specialization in mice, essential for generation of both RORgammat(+) Tregs and T follicular regulatory cells, but not for adipose-resident Tregs. c-Maf is induced in Tregs by IL-6 (show IL6 ELISA Kits) and TGF-beta (show TGFB1 ELISA Kits).
interplay between MATalpha1, c-Myc (show MYC ELISA Kits), and Maf proteins, and their deregulation during chronic cholestasis may facilitate cholangiocarcinoma oncogenesis
MafB and c-Maf have different expression patterns in macrophages, suggesting differences in function.
HERC4 mediates c-Maf ubiquitination and delays growth of multiple myeloma.
Collectively, these studies show that FGF signaling up-regulates expression of alphaA-crystallin (show CRYAA ELISA Kits) both directly and indirectly via up-regulation of c-Maf.
Tec (show NR4A3 ELISA Kits) enhances c-Maf-dependent IL-4 (show IL4 ELISA Kits) promoter activity. This effect of Tec (show NR4A3 ELISA Kits) is counteracted by Ptpn22 (show PTPN22 ELISA Kits), which physically interacts with and facilitates tyrosine dephosphorylation of c-Maf thereby attenuating its transcriptional activity.
endogenous small-Maf factors negatively regulate beta-cell function by competing for MafA binding, and thus, the inhibition of small-Maf activity can improve beta-cell function
The melanoma microenvironment contributes to skewing of CD8 (show CD8A ELISA Kits) T cell differentiation programs, in part by TGFbeta (show TGFB1 ELISA Kits)/IL-6 (show IL6 ELISA Kits)-mediated induction of Maf.
Sox5 (show SOX5 ELISA Kits) physically associates with c-Maf via the HMG (show SSRP1 ELISA Kits) domain of Sox5 (show SOX5 ELISA Kits) and DNA-binding domain of c-Maf, and Sox5 (show SOX5 ELISA Kits) together with c-Maf directly activates the promoter of RORgammat in CD4 (show CD4 ELISA Kits)(+) T cells.
common variant , rs889472, of c-MAF is associated with gout susceptibility.
we identified two heterozygous rare variants in genes that are involved in early cataract development; the novel c.809C>A; p.(Ser270Tyr) in MAF and the c.168C>G; p.(Tyr56 *) variant in CRYGD (show CRYGD ELISA Kits), previously reported as pathogenic
UBE2O mediates c-Maf polyubiquitination and degradation, induces MM cell apoptosis, and suppresses myeloma tumor growth, which provides a novel insight in understanding myelomagenesis and UBE2O biology.
The interaction between c-Maf and RORgammat, and Blimp-1 (show PRDM1 ELISA Kits).
Polymorphisms rs9939609 (FTO (show FTO ELISA Kits) gene) and rs1424233 (MAF gene) were genotyped using allelic discrimination assays in a prospective multicenter cohort study; these polymorphisms did not show associations with birth weight, BMI and Ponderal Index at discharge, and weight gain, neither testing for a dominant, additive nor for a recessive model.
this study shows that genes associated with MAF-binding enhancers are suppressed in macrophages isolated from rheumatoid-arthritis patients, revealing a disease-associated signature of IFN-gamma (show IFNG ELISA Kits)-mediated repression
Our results argued that increased expression of sIL6R from myeloid cells and subsequent c-Maf induction were adverse events for counteracting tumor-specific Th1 (show TH1L ELISA Kits) generation. Overall, this work provides a mechanistic rationale for sIL6R targeting to improve the efficacy of T-cell-mediated cancer immunotherapy
These results define the role of MAF and GSK3 in the resistance of t(14;16) multiple myeloma to proteasome inhibitors.
Epidermal differentiation gene regulatory networks are controlled by MAF and MAFB.
The protein encoded by this gene is a DNA-binding, leucine zipper-containing transcription factor that acts as a homodimer or as a heterodimer. Depending on the binding site and binding partner, the encoded protein can be a transcriptional activator or repressor. This protein plays a role in the regulation of several cellular processes, including embryonic lens fiber cell development, increased T-cell susceptibility to apoptosis, and chondrocyte terminal differentiation. Defects in this gene are a cause of juvenile-onset pulverulent cataract as well as congenital cerulean cataract 4 (CCA4). Two transcript variants encoding different isoforms have been found for this gene.
v-maf musculoaponeurotic fibrosarcoma oncogene homolog (avian)
, V-maf musculoaponeurotic fibrosarcoma oncogene homolog
, c-Maf long form
, proto-oncogene c-maf
, transcription factor Maf
, Avian musculoaponeurotic fibrosarcoma (MAF) protooncogene
, T lymphocyte c-maf long form
, c-maf proto-oncogene
, proto-oncogene c-Maf
, transcription factor Maf-2
, Proto-oncogene c-maf