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Validated All-in-One™ qPCR Primer for ACTB(NM_001101.5) Search again
Product ID:
HQP016381
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BKRNS, BNS, BRWS1, CSMH, DDS1, PS1TP5BP1, THC8
Gene Description:
actin beta
Target Gene Accession:
NM_001101.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes one of six different actin proteins.
Gene References into function
- region responsible for down-regulation of the gamma-actin gene during differentiation is not in the 3' end of the gene in contrast to that for beta-actin.
- human fibroblast cells infected by Cytomegalovirus could express immediate early mRNA and the expression of beta-actin mRNA decreased in a time- and titer-dependent manner
- GLI oncogene is activated through fusion with the beta-actin gene (ACTB) in a group of distinctive pericytic neoplasms
- characterization of the breakpoints of the ACTB-GLI and GLI-ACTB fusions at the genomic level in pericytoma with t(7;12)
- beta-actin localizes to an active U6 promoter in RNA polymerase III (pol III) and is essential for basal pol III transcription.
- both monomeric and oligomeric or polymeric forms of actin are at play and raising the possibility that the equilibrium between them, perhaps differentially regulated at various intranuclear sites, may be a major determinant of nuclear function.
- beta-actin is a transcription factor stimulates eNOS expression; and the transcriptional effect appears to be 27nt-dependent
- Actin could contribute to the initiation of apoptosis by enabling cytosolic pro-apoptotic proteins to be carried to mitochondria by the cytoskeleton-driven trafficking system.
- These findings suggest that mutations in beta actin may be associated with a broad spectrum of developmental malformations and/or neurological abnormalities such as dystonia.
- The results from this controlled CCT-actin folding assay are consistent with a model where CCT and Ac(I) are in a binding pre-equilibrium with a rate-limiting binding step, followed by a faster ATP-driven processing to native actin.
- These data establish that the posttranscriptional event involving HuR-mediated beta-actin mRNA stabilization could be a part of the regulatory mechanisms responsible for maintaining cell integrity.
- Beta-actin can be directly tyrosine-phosphorylated by Src in vitro, and in a Src-dependent manner in cells. Moreover, beta-actin dynamics are suppressed when Src is rendered kinase-inactive.
- The specific and directed rearrangement of the beta-actin structure, seen in the natural beta-actin-TRiC system, is vital for guiding beta-actin to the native state.
- We observed the nuclear translocation of the transcription factor Nrf2 associated with thinning of the actin stress fibers.
- There was no significant difference in IL-4/beta-actin between the patients with AIH and the healthy controls. In contrast there was a significant difference of IFN-gamma/beta-actin between those two groups.