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Mouse Anti-ACTA1 Recombinant Antibody (V2-179482) (CBMAB-A0798-YC)


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Published Data
Mouse Anti-ACTA1 Recombinant Antibody (Alpha Sr-1) (CBMAB-A0798-YC) in IHC
Immunohistochemistry of α-smooth muscle actin of the aortic wall of patients with (a) ascending aortic aneurysm, (b) acute type A aortic dissection, and (c) coronary artery disease showing incremental positivity in aortic media and intima from aortic aneurysm to aortic dissection to coronary artery disease. Arrows indicated the positive reaction of α-smooth muscle actin in the cytoplasma and nucleus. EnVision x200 ...View More
Yuan, S. M., & Wu, N. (2018). Aortic α-smooth muscle actin expressions in aortic disorders and coronary artery disease: An immunohistochemical study. Anatolian Journal of Cardiology/Anadolu Kardiyoloji Dergisi, 19(1).
Mouse Anti-ACTA1 Recombinant Antibody (Alpha Sr-1) (CBMAB-A0798-YC) in IP
The upper band disappeared in C2C12 cells after treatment with 2-D08 (25 μm, 24 h), a small ubiquitin-like modifier (SUMO) E1/E2 ligase inhibitor. DM was administered for 2 days. ...View More
Joung, H., Kwon, S., Kim, K. H., Lee, Y. G., Shin, S., Kwon, D. H., ... & Kook, H. (2018). Sumoylation of histone deacetylase 1 regulates MyoD signaling during myogenesis. Experimental & Molecular Medicine, 50(1), e427-e427.

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat, Rabbit, Chicken
Clone
V2-179482
Antibody Isotype
IgM
Application
IHC, ICC, WB

Basic Information

Immunogen
Purified striated muscle actin from rabbit
Specificity
Human, Mouse, Rat, Rabbit, Chicken
Antibody Isotype
IgM
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
ELISA1:30-1:3,000

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
50 mMol/L Tris-HCl, pH 7.2, 15 mMol/L sodium azide
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Actin, Alpha 1, Skeletal Muscle
Introduction
ACTA1 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 co
Entrez Gene ID
Human58
Rat29437
Mouse11459
Rabbit100009506
Chicken421534
UniProt ID
HumanP68133
RatP68136
MouseP68134
RabbitP68135
ChickenP68139
Alternative Names
Actin, Alpha 1, Skeletal Muscle; Nemaline Myopathy Type 3; ACTA; Actin, Alpha Skeletal Muscle; Alpha-Actin-1; CFTD1; CFTDM; ASMA;
Function
Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells.
Biological Process
Cellular response to organonitrogen compound
Mesenchyme migration
Muscle contraction
Muscle filament sliding
Positive regulation of gene expression
Response to extracellular stimulus
Response to lithium ion
Response to mechanical stimulus
Response to steroid hormone
Skeletal muscle fiber adaptation
Skeletal muscle fiber development
Skeletal muscle thin filament assembly
Cellular Location
Cytoskeleton
Involvement in disease
Nemaline myopathy 3 (NEM3): A form of nemaline myopathy. Nemaline myopathies are muscular disorders characterized by muscle weakness of varying severity and onset, and abnormal thread-like or rod-shaped structures in muscle fibers on histologic examination.
Myopathy, actin, congenital, with excess of thin myofilaments (MPCETM): A congenital muscular disorder characterized at histological level by areas of sarcoplasm devoid of normal myofibrils and mitochondria, and replaced with dense masses of thin filaments. Central cores, rods, ragged red fibers, and necrosis are absent.
Myopathy, congenital, with fiber-type disproportion (CFTD): A genetically heterogeneous disorder in which there is relative hypotrophy of type 1 muscle fibers compared to type 2 fibers on skeletal muscle biopsy. However, these findings are not specific and can be found in many different myopathic and neuropathic conditions.
Myopathy, scapulohumeroperoneal (SHPM): An autosomal dominant muscular disorder characterized by progressive muscle weakness with initial scapulo-humeral-peroneal and distal distribution. Over time, muscle weakness progresses to proximal muscle groups. Clinical characteristics include scapular winging, mild lower facial weakness, foot drop due to foot eversion and dorsiflexion weakness, and selective muscle atrophy. Age at onset and disease progression are variable.
PTM
Oxidation of Met-46 and Met-49 by MICALs (MICAL1, MICAL2 or MICAL3) to form methionine sulfoxide promotes actin filament depolymerization. MICAL1 and MICAL2 produce the (R)-S-oxide form. The (R)-S-oxide form is reverted by MSRB1 and MSRB2, which promotes actin repolymerization.
Monomethylation at Lys-86 (K84me1) regulates actin-myosin interaction and actomyosin-dependent processes. Demethylation by ALKBH4 is required for maintaining actomyosin dynamics supporting normal cleavage furrow ingression during cytokinesis and cell migration.
Methylated at His-75 by SETD3.
(Microbial infection) Monomeric actin is cross-linked by V.cholerae toxins RtxA and VgrG1 in case of infection: bacterial toxins mediate the cross-link between Lys-52 of one monomer and Glu-272 of another actin monomer, resulting in formation of highly toxic actin oligomers that cause cell rounding. The toxin can be highly efficient at very low concentrations by acting on formin homology family proteins: toxic actin oligomers bind with high affinity to formins and adversely affect both nucleation and elongation abilities of formins, causing their potent inhibition in both profilin-dependent and independent manners.
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For research use only. Not intended for any clinical use.

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