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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.
ACTA2 Arg179 alterations cause a chronic condition presenting in infancy and requiring life-long surveillance and treatment. Affected individuals are at risk of acute events due to aortic dissection or rupture, arterial thrombosis, ischemic stroke and pulmonary complications.
Study found that alphaSMA expression is associated with the survival of ER(+) breast cancer patients. Also study observed that wildtype TP53 upregulates alphaSMA expression in tamoxifenresistant breast cancer cells.
Ki67 LI, CD105, and alpha-SMA expression showed significant differences between normal, low-risk oral epithelial dysplasia and high-risk oral epithelial dysplasia. These findings further support that features such as increased basal cell layer hyperplasia, abnormal superficial mitosis, increased nuclear-cytoplasmic ratio, and hyperchromasia could be transformation-relevant dysplastic features.
Adenocarcinomas showed significantly higher staining scores of both VEGF and alphaSMA than squamous cell carcinomas did. In 42 cases of high CD31 score, five-year survival rate (87%) of patients with lung cancer showing mature tumor vessels was significantly better than that (69%) of patients with immature tumor vessels
connective tissue disease including ACTA2 mutations should be considered for aortic dissection in young adult patients.
cellular defects due to the ACTA2 mutation in both aortic smooth muscle cells and adventitial fibroblasts may contribute to development of thoracic aortic aneurysms and dissections and proliferative occlusive vascular disease
our results seemed to justify the conclusion that ACTA2 did not play a significant role in the pathogenesis of BAV aortopathy.
In patients with MYH11 or ACTA2 variants, the effect of intronic variants on splicing was demonstrated on the mRNA level in the induced smooth muscle cell (SMC), allowing classification into pathogenic or nonpathogenic variants.
We present a young woman whose ACTA2 mutation was ascertained during pregnancy because of her father's history of dissecting aneurysms. She was delivered at full term by cesarean section and subsequently had severe uterine hemorrhage due to uterine atony. Targeted analysis of the patient's ACTA2 gene revealed she had inherited the N117S variant from her father.
During transition from the pluripotent stage towards the neural developmental stage, ACTA2 is differentially expressed in bipolar patient derived cells compared to control derived cells.
Two unrelated patients with the heterozygous R189H mutation in ACTA2 and complex congenital heart defects expands the cardiac phenotype of multisystemic smooth muscle dysfunction syndrome.
Cells in high glucose for 7 days showed a significant decrease in mRNA expression of CD31 and VE-cadherin, and a significant increase in that of alpha-SMA and collagen I.
ACTA2 is the isoform of contractile protein alpha-actin present in vascular smooth muscle cells (SMCs) throughout the arterial tree.4 Pathologic conditions in individuals with ACTA2 mutations show increased deposition of SMCs in the intimal arterial layer, leading to a decreased intraluminal diameter.4
Two novel actin alpha 2 mutations (N117I and L348R) were identified in each familial non-syndromatic thoracic aortic aneurysm proband separately, and an additional novel actin alpha 2 mutation (Y168N) was identified in one patient with sporadic non-syndromatic thoracic aortic aneurysm.
The R179H mutation has the potential to affect actin structure and function in both the contractile domain of the cell and the more dynamic cytoskeletal pool of actin, both of which are required for contraction.
site-directed mutagenesis revealed several basic amino acid residues in the intermolecular (R267) and intramolecular (K82 and R159) subdomains that are essential for Purbeta transcriptional repressor function in Acta2 promoter-reporter assays. In keeping with their diminished Acta2 repressor activity in fibroblasts, purified Purbeta variants containing an R267A mutation exhibited reduced binding affinity for purine-ric...
Data show that the expression profiles of three proteins: E-cadherin, Snail, and alpha-smooth muscle actin were significantly different in extraprostatic extension prostate cancer (PCa) compared with intra-prostatic tumour.
ACTA2 mutations are associated with structural disruption and functional impairment of contractile proteins, and predispose to a variety of diffuse vascular diseases including TAAD, CAD, ischemic strokes, and Moyamoya disease. Vascular SMCs are also implicated in vascular remodeling in both physiological and pathological conditions.
Parenchymal alphaSMA expression in hepatic tissue appeared to increase only among hepatitis C subjects with fibrosis 3-4.
Multisystemic smooth muscle dysfunction syndrome secondary to an ACTA2 mutation.
These data revealed that Rho GTPase signaling is required for TGF beta-induced expression of alpha-smooth muscle actin (alphaSMA) but not of collagen I alpha1 (col1a1).
In murine myocardial infarction, infiltration of the infarct border zone with abundant a-SMA-positive myofibroblasts was associated with scar contraction. Isolated cardiac fibroblasts cultured in plates showed high a-SMA expression localized in stress fibers, exhibited activation of focal adhesion kinase (FAK), and synthesized large amounts of extracellular matrix proteins.
These data suggest that the interplay between cell-matrix adhesion and intercellular adhesion is an important determinant for some aspects of TGFbeta1-induced epithelial-mesenchymal transition via alphaSMA expression induction.
The level of alpha-SMA expression by intramuscular fibrogenic cells does not correlate positively with the level of collagen gene expression or the severity of skeletal muscle fibrosis in the mdx5cv mice. alpha-SMA is not a functional marker of fibrogenic cells in skeletal muscle fibrosis associated with muscular dystrophy
Data suggest that membrane-proximal signaling complexes constrained by AKAP220 impact the actin barrier dynamics and AQP2 trafficking to ensure water homeostasis.
Gremlin1 accelerates hepatic stellate cell activation through upregulation of TGF-B1, alpha-SMA, and COL1a1 expression in a liver fibrosis disease model.
Disruption of smooth muscle Acta2 increases reactive oxygen species levels, activates NF-kappaB signaling and increases AngII receptor type I a expression.
The expression levels of alpha-smooth muscle actin (alpha-SMA, a marker of fibroblast activation) in fibrotic livers were significantly higher than those in control livers.
this study identifies Rac1 as a downstream target for SMA to inhibit smooth muscle cell proliferation and migration.
the coordinated up-regulations of desmin and alpha- actinin specifically in the early stage of diastolic heart failure mouse models indicate a novel myocardial response.
Alpha-smooth muscle actin protein and mRNA are enhanced from brain blood vessels in an Alzheimer's disease animal model.
Astragaloside can delay the renal fibrosis process in diabetic mice by influencing the TGF-beta/SMADS signaling pathway and down-regulating TGF-beta1, SMAD2/3, and alpha-SMA expression.
The increased expressions of the cartilage-associated proteins Collagen2 and alpha-SMA during scleral chondrogenesis accompany myopia development.
Results suggest that the atypical motif asparaging-cysteine-systeine Asn(17)-Cys(18)-Cys(19) is crucial for the normal surface trafficking and function of hydroxycarboxylic acid receptor 2 protein hGPR109A.
The results suggest that the expression level of TGF-b1 and a-SMA in stromal fibroblasts may have prognostic significance in patients with clinical stage I-IIIA NSCLC after curative resection
alphaSMA is a useful marker for further understanding the molecular and cellular characteristics of non-hematopoietic cells in the lymph nodes.
This in vitro expression study revealed the additional profibrotic role of IL-6 in fibroblast to myofibroblast transition and in alpha smooth muscle actin induction.
Data indicate that NRG-1beta up-regulated the gene expressions of Nkx2.5, GATA4, alpha-actin, MLC-2v, and ANF in a time-dependent regulation of ErbB/ERK1/2 pathways.
TnT has a previously unrecognized role in forming the inactive state of regulated actin.
The terminal pointed end subunit is tilted towards the penultimate subunit, allowing specific and extra loop-to-loop inter-strand contacts between the two end subunits, which is not possible in other parts of the filament.
There was no significant change in the expression of TGF-beta(2) and alpha-SMA after laser-assisted intrastromal scanning.
The arrangement of actin subunits in an actin dimer assembled by tandem W domains resembles that of a long-pitch helix of the actin filament.
The distribution of laminin and alphaSMA in the testis and epididymis might point out to their roles in the male reproduction.
The protein encoded by this gene belongs to the actin family of proteins, which are highly conserved proteins that play a role in cell motility, structure and integrity. Alpha, beta and gamma actin isoforms have been identified, with alpha actins being a major constituent of the contractile apparatus, while beta and gamma actins are involved in the regulation of cell motility. This actin is an alpha actin that is found in skeletal muscle. Defects in this gene cause aortic aneurysm familial thoracic type 6. Multiple alternatively spliced variants, encoding the same protein, have been identified.
, alpha smooth muscle actin
, actin, alpha 2, smooth muscle, aorta
, actin alpha cardiac 1
, actin, aortic smooth muscle
, vascular smooth muscle alpha-actin
, alpha-smooth muscle actin
, actin, aortic smooth muscle-like
, alpha-cardiac actin
, cell growth-inhibiting gene 46 protein
, actin, alpha, vascular smooth muscle
, alpha actin 2
, smooth muscle alpha-actin
, alpha actin