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Mouse Monoclonal Anti-beta-Actin antibody (STJ99027)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, ELISA
Recommended dilution: WB 1:500-2000; ELISA 1:10000-20000
Recommended protocols: check protocols
Click or hover above images to see image description for Anti-beta-Actin antibody.
Check alternative names for the antibodyExpand
SCBT cat No:
|Catalogue No.|| |
Human, Rat, Mouse, Goat, Monkey, Hamster
Anti-beta-Actin antibody detects endogenous levels of beta actin and does not cross-react with related proteins.
Purified recombinant human beta actin protein fragments expressed in E.coli.
|Recommended dilution|| |
WB 1:500-2000; ELISA 1:10000-20000
|Molecular weight|| |
Anti-beta-Actin antibody was tube-contained in liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Anti-beta-Actin antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Database links|| |
|Protein function|| |
Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells.
|Involvement in disease|| |
Dystonia, juvenile-onset (DJO) [MIM:607371]: A form of dystonia with juvenile onset. Dystonia is defined by the presence of sustained involuntary muscle contraction, often leading to abnormal postures. Patients with juvenile-onset dystonia manifest progressive, generalized, dopa-unresponsive dystonia, developmental malformations and sensory hearing loss. . Note=The disease is caused by mutations affecting the gene represented in this entry.; Baraitser-Winter syndrome 1 (BRWS1) [MIM:243310]: A rare developmental disorder characterized by the combination of congenital ptosis, high-arched eyebrows, hypertelorism, ocular colobomata, and a brain malformation consisting of anterior-predominant lissencephaly. Other typical features include postnatal short stature and microcephaly, intellectual disability, seizures, and hearing loss. . Note=The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the actin family.
|Protein post-translational modifications|| |
ISGylated. .; Oxidation of Met-44 and Met-47 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 promote actin repolymerization (By similarity). .; Monomethylation at Lys-84 (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. .; (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-50 of one monomer and Glu-270 of another actin monomer, resulting in formation of highly toxic actin oligomers that cause cell rounding (PubMed:19015515). 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 (PubMed:26228148). .
|Protein cellular localization|| |
Cytoplasm, cytoskeleton . Note=Localized in cytoplasmic mRNP granules containing untranslated mRNAs.
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St John’s Laboratory Ltd.
|Product type|| |
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