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The protein encoded by MKL1 interacts with the transcription factor myocardin, a key regulator of smooth muscle cell differentiation. 再加上，我们可以发MKL1 抗体 (81) 和 和数多这个蛋白质的别的产品。
TNF-alpha (显示 TNF ELISA试剂盒) and LPS (显示 IRF6 ELISA试剂盒) promoted the interaction between MKL1 and PCAF (显示 KAT2B ELISA试剂盒).
MRTF-A-miR (显示 MLXIP ELISA试剂盒)-206-WDR1 (显示 WDR1 ELISA试剂盒) form feedback loop to regulate breast cancer cell migration.
miR (显示 MLXIP ELISA试剂盒)-93-5p regulates myocardin-like (显示 MYOCD ELISA试剂盒) 1 and STAT3 (显示 STAT3 ELISA试剂盒) to affect epithelial-mesenchymal transition controlling breast cancer cell migration
results highlight the critical role of the actin-regulated MRTF transcriptional pathway for bleb-associated invasive motility, such as during entosis.
transcriptional co-activator MRTF-A and actin polymerization regulated a subset of miRNAs in vascular smooth muscle. Identification of novel miRNAs regulated by actin/MRTF-A may provide further insight into the mechanisms underlying vascular disease states, such as aortic aneurysm, as well as novel ideas regarding therapeutic strategies
Data suggest 2 major isoforms of profilin (Pfn1 and Pfn2) are co-regulated by a common mechanism involving the action of MKL1 [megakaryoblastic leukemia (translocation) 1 protein] that is independent of its SRF- (serum-response factor)-related activity; cellular externalization of Pfn1, rather than transcription, is affected by the perturbations of MKL1; MKL1 can influence cell migration by modulating Pfn1 expression.
RBM15-MKL1 fusion is associated with acute megakaryoblastic leukemia in non-Down syndrome.
The authors show MRTF family proteins bind YAP (显示 YAP1 ELISA试剂盒) via a conserved PPXY motif that interacts with the YAP (显示 YAP1 ELISA试剂盒) WW domain (显示 DRP2 ELISA试剂盒). This interaction allows MRTF to recruit NcoA3 (显示 NCOA3 ELISA试剂盒) to the TEAD-YAP (显示 YAP1 ELISA试剂盒) transcriptional complex and potentiate its transcriptional activity.
The MKL1 promotes ovarian cancer cell migration and invasion by epigenetically activating MMP2 (显示 MMP2 ELISA试剂盒) transcription.
Data suggest an interplay between megakaryocytic leukemia 1 (MKL1) and ASH2 protein to promote tumor necrosis factor alpha (TNF-alpha (显示 TNF ELISA试剂盒)) induced proinflammatory transcription in macrophages.
beta-catenin (显示 CTNNB1 ELISA试剂盒) controls myocardin (显示 MYOCD ELISA试剂盒)-related transcription factor-dependent transcription and emerges as a critical regulator of an array of cytoskeletal genes.
Here, the authors show that Rho-dependent MRTF phosphorylation reflects its nuclear accumulation and dissociation from G-actin (显示 ACTB ELISA试剂盒), and identify multiple sites for MRTF phosphorylation, which contribute to transcriptional activation.
BRG1 promotes transcription of endothelial Mrtfa and Mrtfb, which elevates expression of SRF and SRF target genes that establish embryonic capillary integrity.
knockdown of MKL1 induces a significant increase in the transcriptional activity of PPARgamma (显示 PPARG ELISA试剂盒) target genes and MKL1 interacts with PPARg (显示 PPARG ELISA试剂盒), suggesting that SRF and MKL1 independently inhibit brown adipogenesis and that MKL1 exerts its effect mainly by modulating PPARgamma (显示 PPARG ELISA试剂盒) activity
further found that hypericin ameliorates inflammatory response by suppressing MKL1, which is the essential cofactor of p65 (显示 NFkBP65 ELISA试剂盒) during the transcription process. In an Abeta (显示 APP ELISA试剂盒) 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 (显示 RHOA ELISA试剂盒)/MRTF-A luciferase reporter.
MRTF-A regulates liver fibrosis by epigenetically tuning the TGF-beta (显示 TGFB1 ELISA试剂盒) 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.
MRTF-A is a critical for epithelial to mesenchymal transition and can be stereoselectively inhibited by CCG-1423.
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.
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