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Heterozygous deletional mutation (c.5803delG) in exon 41 of the MYH9 gene is associated with inherited thrombocytopenia.
cytokinesis failure in megakaryocytes is the consequence of both the absence of NMIIB and a low RhoA activity that impairs NMIIA localization at the cleavage furrow through increased actin turnover.
The loss of junctional NMIIA, upon Coronin 1B (show CORO1B Proteins) knockdown, perturbed RhoA (show RHOA Proteins) signaling.
Results identified nonsynonymous variants in MYH9 and ABCA4 (show ABCA4 Proteins) to be the most frequent risk loci in nonsyndromic orofacial clefts in the Taiwanese population.
Our study is the first to identify genetic predisposition to transplant renal artery stenosis in patients with MYH9 risk allelic variants (rs4821480, rs4821481, rs3752462, rs11089788, rs136211, rs5756168, rs2032487, and rs2239784)
The hearing impairment associated with MYH9 disorder in this family was characterized as adult onset, progressive, and high-frequency dominant. Hematological manifestations of MYH9 disorder show complete penetrance, whereas extra-hematological manifestations show incomplete penetrance and variable expressivity in this family.
mass spectrum followed by immunoprecipitation identified non-muscle myosin heavy chain-IIA (NMMHC-IIA) as the CXCR4 (show CXCR4 Proteins)-interacting protein. Furthermore, pharmaceutical inhibition of NMMHC-IIA by blebbistatin dampened the nuclear translocation of CXCR4 (show CXCR4 Proteins) as well as the metastatic capacity of RCC (show XRCC1 Proteins) cells
The rs3752462 polymorphism of MYH9 is associated with high systolic blood pressure in patients with CKD. The T allele in the dominant model was associated with an elevated risk for high systolic blood pressure .
The Raf-ERK1/2 signaling pathway is involved in regulation of NMIIA by DT-13.
HhnRNP-K-mediated regulation of NMHC IIA mRNA translation contributes to the control of enucleation in erythropoiesis.
Data show that the locomotion and blebbing of the primordial germ cells (PGCs) required F-actin, myosin II activity and RhoA/Rho-associated protein kinase (ROCK) signaling.
APPL1 (show APPL1 Proteins) enhances glucose uptake by modulating the activation and localization of PKCzeta (show PRKCZ Proteins), as well as its functional interaction with both PP2A (show PPP2R2B Proteins) and myosin IIa.
Data show that deletion of myosin heavy chain II-A (Myh9)/myosin heavy chain II-B (Myh10) caused severe hydroureter/hydronephrosis at birth.
our data indicated that PGDHC is a Pg-derived, cell-permeable ceramide that possesses a unique property of promoting osteoclastogenesis via interaction with Myh9 which, in turn, activates a Rac1/DC-STAMP pathway for upregulation of osteoclast cell fusion.
Conditional deletion of nonmuscle myosin II-A in mouse tongue epithelium results in squamous cell carcinoma
Inhibition of NMMHC IIA impedes TF expression and venous thrombosis via Akt (show AKT1 Proteins)/GSK3beta-NF-kappaB (show NFKB1 Proteins) signalling pathways in the endothelium both in vitro and in vivo.
Myh9 mediates colitis-induced epithelium injury by restricting Lgr5 (show LGR5 Proteins)+ stem cells
Mst1 (show MST1 Proteins) regulates Myosin IIa dynamics to organize high and low affinity LFA-1 (show ITGAL Proteins) to the anterior and posterior membrane during T cell migration.
DDR1 malfunction causes outer hair cells deformation and the separation of the lateral wall, the location of the cellular motor responsible for the electromotile property, explicitly in those regions showing DDR1 and NM-IIA co-localization.
A new role for Arl13b (show ARL13B Proteins) in actin cytoskeleton remodeling through the interaction with Myh9.
Lgl1 (show Klra7 Proteins) forms two distinct complexes in vivo, Lgl1 (show Klra7 Proteins)-NMIIA and Lgl1 (show Klra7 Proteins)-Par6alpha (show PARD6A Proteins)-aPKCzeta (show PRKCZ Proteins), and that the formation of these complexes is affected by the phosphorylation state of Lgl1 (show Klra7 Proteins).
Results demonstrate an important role of NMHC-IIA for the proper formation and function of the glomerulus in zebrafish.
This gene encodes a conventional non-muscle myosin\; this protein should not be confused with the unconventional myosin-9a or 9b (MYO9A or MYO9B). The encoded protein is a myosin IIA heavy chain that contains an IQ domain and a myosin head-like domain which is involved in several important functions, including cytokinesis, cell motility and maintenance of cell shape. Defects in this gene have been associated with non-syndromic sensorineural deafness autosomal dominant type 17, Epstein syndrome, Alport syndrome with macrothrombocytopenia, Sebastian syndrome, Fechtner syndrome and macrothrombocytopenia with progressive sensorineural deafness.
cellular myosin heavy chain, type A
, myosin heavy chain 9
, myosin heavy chain, non-muscle IIa
, non-muscle myosin heavy chain A
, non-muscle myosin heavy chain IIa
, non-muscle myosin heavy polypeptide 9
, nonmuscle myosin heavy chain II-A
, NMMHC II-a
, myosin, heavy polypeptide 9, non-muscle
, nonmuscle myosin heavy chain-A
, heavy polypeptide 9
, myosin heavy chain, nonmuscle
, non-muscle IIa
, type A
, nonmuscle myosin II heavy chain A
, myosin IIA
, myosin heavy chain IX
, myosin, heavy chain 9, non-muscle, like-2