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MEF2D is a member of the myocyte-specific enhancer factor 2 (MEF2) family of transcription factors. 再加上，我们可以发MEF2D 蛋白 (6) 和 MEF2D 试剂盒 (2)和数多这个蛋白质的别的产品。
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Human Polyclonal MEF2D Primary Antibody for IHC - ABIN966557
Breitbart, Liang, Smoot, Laheru, Mahdavi, Nadal-Ginard: A fourth human MEF2 transcription factor, hMEF2D, is an early marker of the myogenic lineage. in Development (Cambridge, England) 1994
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Human Polyclonal MEF2D Primary Antibody for IHC - ABIN966558
Zhao, New, Kravchenko, Kato, Gram, di Padova, Olson, Ulevitch, Han: Regulation of the MEF2 family of transcription factors by p38. in Molecular and cellular biology 1999
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Dog (Canine) Monoclonal MEF2D Primary Antibody for IF, IP - ABIN968169
Guttridge, Mayo, Madrid, Wang, Baldwin: NF-kappaB-induced loss of MyoD messenger RNA: possible role in muscle decay and cachexia. in Science (New York, N.Y.) 2000
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Dog (Canine) Monoclonal MEF2D Primary Antibody for IF, IP - ABIN968170
Martin, Miano, Hustad, Copeland, Jenkins, Olson: A Mef2 gene that generates a muscle-specific isoform via alternative mRNA splicing. in Molecular and cellular biology 1994
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MEF2D might be a potential biomarker during chronic inflammation-lung cancer transition, predicting the risk of lung cancer among patients with chronic respiratory diseases.
HIF-1alpha (显示 HIF1A 抗体) transactivates MEF2D expression by binding to the MEF2D gene promoter to induce angiogenesis in colorectal tumors.
MEF2D directly regulated transcription of the epithelial-mesenchymal transition driver gene ZEB1 (显示 ZEB1 抗体) and facilitated histone acetylation at the ZEB1 (显示 ZEB1 抗体) promoter in colorectal cancer cells
MEF2D-BCL9 (显示 BCL9 抗体)-positive patients had B-cell precursor immunophenotype and were characterized as being older in age, being resistant to chemotherapy, having very early relapse, and having leukemic blasts that mimic morphologically mature B-cell leukemia with markedly high expression of HDAC9 (显示 HDAC9 抗体).
These results suggest that PPARgamma (显示 PPARG 抗体) may exert its antiproliferative effects by negatively regulating the MEF2D in CM cells, which through upregulation of miR (显示 MLXIP 抗体)-122, and PPARgamma (显示 PPARG 抗体)/miR (显示 MLXIP 抗体)-122/MEF2D signaling pathway may be a novel target for treatment of CM.
MEF2D overexpression participated in the growth of lung cancers and its aberrant expression may result from the reduction of tumor suppressor miR (显示 MLXIP 抗体)-218.
MEF2D is a direct target of miR (显示 MLXIP 抗体)-19.
We found that in malignant glioma, there is an aberrantly high expression of MEF2D, which leads to poor prognosis of malignant glioma. The downregulation of MEF2D suppresses the proliferation of malignant glioma cell lines by inducing delay of S and G2/M phases of cell cycle and promoting apoptosis.
MEF2D regulates IGF-1 (显示 IGF1 抗体)-induced proliferation and apoptosis in CM development, indicating IGF-1 (显示 IGF1 抗体)-MEF2D pathway may be a useful target for treatment.
Pokemon (显示 ZBTB7A 抗体) was found to enhance the migration and invasion of hepatocellular carcinoma by increasing MEF2D expression
These findings uncover a novel role for Mef2c (显示 MEF2C 抗体)/d in coordinating the transcriptional network that promotes early B-cell development.
This study identifies MEF2D as a critical regulator of IL-10 (显示 IL10 抗体) gene expression that negatively controls microglia inflammation response and prevents inflammation-mediated cytotoxicity.
Mef2d is essential for the maturation and integrity of retinal photoreceptor and bipolar cells
miR (显示 MLXIP 抗体)-103 worked through activating AKT (显示 AKT1 抗体)/mTOR (显示 FRAP1 抗体) signal pathway and impairing target gene MEF2D.
These findings demonstrate that broadly expressed TFs acquire specific functions through competitive recruitment to enhancers by tissue-specific Mef2d and through selective activation of these enhancers to regulate tissue-specific genes.
Whereas MEF2A (显示 MEF2A 抗体) is absolutely required for proper myoblast differentiation, MEF2B (显示 MEF2B 抗体), -C, and -D were found to be dispensable for this process.
A role for endogenous MEF2 (显示 MEF2C 抗体) factors exclusively in hormone/Fsk/cAMP-induced Nr4a1 (显示 NR4A1 抗体) gene expression in mouse MA-10 Leydig cells.
Oxidation of survival factor MEF2D inhibits its function, underlies oxidative stress-induced (显示 SQSTM1 抗体) neurotoxicity, and may be a part of the Parkinson disease pathogenic process.
Results demonstrate that coordinated alternative splicing by a single RNA binding protein modulates transcription (Mef2d) and cell signaling (Rock2 (显示 ROCK2 抗体)) programs to drive tissue-specific functions (cell fusion) to promote a developmental transition.
We found that Parkinson's disease -associated neurotoxins destabilize MEF2D mRNA and reduce its level in vitro and in vivo.
Expression analysis showed that the MEF2D polymorphisms were highly correlated with MEF2D mRNA and protein levels in the longissimus dorsi muscle of Polish Holstein-Friesian bulls carrying the three different combined genotypes.
This gene is a member of the myocyte-specific enhancer factor 2 (MEF2) family of transcription factors. Members of this family are involved in control of muscle and neuronal cell differentiation and development, and are regulated by class II histone deacetylases. Fusions of the encoded protein with Deleted in Azoospermia-Associated Protein 1 (DAZAP1) due to a translocation have been found in an acute lymphoblastic leukemia cell line, suggesting a role in leukemogenesis. The encoded protein may also be involved in Parkinson disease and myotonic dystrophy. Alternative splicing results in multiple transcript variants.
myocyte enhancer factor 2D
, MADS box transcription enhancer factor 2, polypeptide D (myocyte enhancer factor 2D)
, myocyte-specific enhancer factor 2D-like
, MADS box transcription enhancer factor 2, polypeptide D
, myocyte-specific enhancer factor 2D