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Acts as a transcriptional coactivator of serum response factor (SRF). Additionally we are shipping MKL2 Antibodies (25) and and many more products for this protein.
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While disruption of the MKL2:SRF axis has been associated with severe microcephaly and disordered brain development in multiple model systems, the role of this transcription factor complex has not been previously demonstrated in human brain development.
There were multiple independent HIV integrations in several genes, including MKL2 and BACH2 (show BACH2 Proteins); many of these integrations were in clonally expanded cells.
MKL1/2 depletion resulted in Ras activation, elevated p16 expression and hypophosphorylation of the retinoblastoma (Rb) protein in DLC1-deficient hepatocellular carcinoma cells.
Based on a recurrent translocation t(11;16)(q13;p13), the C11orf95-MKL2 fusion gene has been found in eight further cases of chondroid lipomas.
study provides evidence that MKL1/2 mediates cancerous transformation in DLC1-deficient hepatocellular and mammary carcinoma cells
C11orf95-MKL2 is the resulting fusion oncogene (show RAB1A Proteins) of t(11;16)(q13;p13) in chondroid lipoma.
dominant negative MKL2 blocked differentiation-induced expression of SRF target genes skeletal alpha-actin and alpha-myosin heavy chain and blocked differentiation of the myoblasts to myotubes in vitro.
BMP signaling modulates VSMC phenotype via cross-talk with the RhoA/MRTFs pathway, and may contribute to the development of the pathological characteristics observed in patients with PAH and other obliterative vascular diseases.
Myocardin-related transcription factors are critical mediators of transforming growth factor beta (TGF-beta) 1-induced epithelial-mesenchymal transition.[
RNA interference was used to investigate the contribution of the MRTF-SRF pathway to cytoskeletal dynamics in MDA-MB-231 breast carcinoma and B16F2 melanoma cells, in which basal MRTF-SRF activity is Rho-dependent.
MRTF-A/B depletion results in an increase in the cell surface expression of ICAM-1 (show ICAM1 Proteins) and interactions between HAoECs and leukocytes
Either MRTF-A or MRTF-B is dispensable for cardiac development, whereas deletion of both causes a spectrum of abnormalities ranging from reduced cardiac contractility and adult onset heart failure to neonatal lethality accompanied by sarcomere disarray.
These results identify SRF and its MRTF cofactors as major transcriptional regulators of endothelial cell junctional stability, guaranteeing physiological functions of the cerebral microvasculature.
Suggest role for nuclear RhoA (show RHOA Proteins) signaling in MRTF-dependent gene expression in smooth muscle cells.
Myocardin-related transcription factor (MRTF)-A and MRTF-B (MKL1 and MKL2, respectively) are enriched in the perinuclear space of epicardial cells during development.
MKL1/2 and ELK4 co-regulate distinct serum response factor (SRF) transcription programs in macrophages.
Smad2 (show SMAD2 Proteins) interaction with MRTFB seems to be a novel and important mechanism underlying neural crest cell differentiation to vascular smooth muscle cells.
MRTF-B knockdown leads to increase in S and G2/M populations and downregulation of cyclin (show PCNA Proteins)-CDK (show CDK4 Proteins) inhibitors p27Kip1 (show CDKN1B Proteins), p18Ink4c (show CDKN2C Proteins) and 19Ink4d as well as upregulation of p21Waf1 and cyclin D1 (show CCND1 Proteins).
Data suggest that MKL1 and MKL2 are expressed in megakaryocytes and platelets; megakaryocytes lacking expression of MKL1 and/or MKL2 have both defective megakaryocytopoiesis and thrombopoiesis.
MKL2 regulates a conserved TGF-beta (show TGFB1 Proteins) signaling pathway that is required for angiogenesis and ultimately embryonic survival.
Acts as a transcriptional coactivator of serum response factor (SRF). Required for skeletal myogenic differentiation.
, megakaryoblastic leukemia 2 protein
, MKL/myocardin-like protein 2
, megakaryoblastic leukemia 2
, myocardin-related transcription factor B
, gene trap insertion site 4-1