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The protein encoded by MKL1 interacts with the transcription factor myocardin, a key regulator of smooth muscle cell differentiation. Additionally we are shipping MKL1 Antibodies (76) and and many more products for this protein.
Data suggest an interplay between megakaryocytic leukemia 1 (MKL1) and ASH2 protein to promote tumor necrosis factor alpha (TNF-alpha (show TNF ELISA Kits)) induced proinflammatory transcription in macrophages.
The results suggest that integrin-adhesion-induced MRTF-A-SRF activation and ISG15 (show ISG15 ELISA Kits) expression constitute a newly discovered signaling circuit that promotes cell migration and invasion.
Study showed that MRTF-A and MRTF-B were upregulated in pancreatic cancer tissues supporting the hypothesis that both of them are oncogenes in pancreatic cancer.
FLNA (show FLNA ELISA Kits) functions as a positive cellular transducer linking actin polymerization to MKL1-SRF activity, counteracting the known repressive complex of MKL1 and monomeric G-actin (show ACTB ELISA Kits).
Redox-sensitive regulation of MRTF-A phosphorylation via palladin (show PALLD ELISA Kits) in vascular smooth muscle cell differentiation marker gene expression.
Identification of SAP (show APCS ELISA Kits)-dependent Mkl1 signaling as a previously unrecognized mediator of aggressive progression of mammary tumors locally relapsing after radiotherapy.
MRTF-A is a critical for epithelial to mesenchymal transition and can be stereoselectively inhibited by CCG-1423.
p300 (show EP300 ELISA Kits) and MRTF-A synergistically enhance the expression of migration-related genes in breast cancer cells.
Myocardin-Related Transcription Factor A and Yes-Associated Protein Exert Dual Control in G protein-coupled receptor (show ADRA1A ELISA Kits)- and RhoA (show RHOA ELISA Kits)-mediated transcriptional regulation and cell proliferation
Study found that MRTF-A expression was up-regulated in metastatic anaplastic thyroid cancer tissues and promoted metastasis-relevant traits in vitro.
beta-catenin (show CTNNB1 ELISA Kits) controls myocardin (show MYOCD ELISA Kits)-related transcription factor-dependent transcription and emerges as a critical regulator of an array of cytoskeletal genes.
further found that hypericin ameliorates inflammatory response by suppressing MKL1, which is the essential cofactor of p65 (show NFkBP65 ELISA Kits) during the transcription process. In an Abeta (show APP ELISA Kits) injection AD mouse model, animals orally administrated hypericin (50 mg/kg) for seven days significantly decreased pro-inflammatory cytokines expression and NO production in hippocampus, meanwhile, hypericin improved oAbeta42-induced learning and memory...
Study demonstrates that WH2 domains activate MRTF-A and contribute to target gene regulation by a competitive mechanism, independently of their role in actin filament formation.
The transcriptional co-activator MRTF-A was activated by sphingosine-1-phosphate as assessed by its nuclear accumulation and induction of a RhoA (show RHOA ELISA Kits)/MRTF-A luciferase reporter.
MRTF-A regulates liver fibrosis by epigenetically tuning the TGF-beta (show TGFB1 ELISA Kits) signaling pathway in HSCs
Exploration of the molecular causes of enhanced cardiac hypertrophy revealed significant activation of beta-catenin/GSK-3beta signaling, whereas MAPK and MKL1/serum-response factor pathways were inhibited.
MKL1 plays a significant role in mediating the fibrotic response to bleomycin injury. Loss of MKL1 attenuated early neutrophil influx, as well as myofibroblast-mediated remodeling.
MRTF-A/B depletion results in an increase in the cell surface expression of ICAM-1 (show ICAM1 ELISA Kits) and interactions between HAoECs and leukocytes
knockdown of MRTF-A synthesis abolishes the systemic sclerosis myofibroblast enhanced basal contractility and synthesis of type I collagen and inhibits the matricellular profibrotic protein, connective tissue growth factor (CCN2/CTGF (show CTGF ELISA Kits)
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.
The protein encoded by this gene interacts with the transcription factor myocardin, a key regulator of smooth muscle cell differentiation. The encoded protein is predominantly nuclear and may help transduce signals from the cytoskeleton to the nucleus. This gene is involved in a specific translocation event that creates a fusion of this gene and the RNA-binding motif protein-15 gene. This translocation has been associated with acute megakaryocytic leukemia.
megakaryoblastic leukemia 1 protein
, MKL/myocardin-like protein 1
, RNA-binding motif protein 15/megakaryoblastic leukemia-1 fusion protein
, basic, SAP and coiled-coil domain
, megakaryocytic acute leukemia protein
, myocardin-related transcription factor A
, basic SAP and coiled-coil domains
, basic SAP coiled-coil transcription activator
, megakaryoblastic leukemia (translocation) 1 homolog
, megakaryoblastic leukemia 1 protein homolog