Disease relevance of Actb

• Therefore, a recombinant retrovirus allowing expression of the TNF gene by the beta-actin promotor has been constructed and used to infect the two tumor cell lines EB and ESB, which grow as solid tumor or metastasize, respectively [1].
• Using transient cotransfection assays, ZF5 was shown to activate the HIV-1 LTR and repress the beta-actin promoter [2].
• Promoters tested included those of alpha-actin (alpha A775), beta-actin (beta A280), cytochrome oxidase (CO1250 and CO650), myogenin (Mg1031 and Mg353), and Rous sarcoma virus (RSV). beta A200, which was derived from beta A280 by eliminating potential polyadenylation sites, was also tested [3].
• To test the hypothesis that IGFBP-5 promotes the acquisition of bone mineral density (BMD), we generated transgenic (Tg) mice overexpressing Igfbp5 using a cytomegalovirus enhancer and beta-actin promoter (CMV/betaA) [4].
• In this work, the most reliable housekeeping gene for gene expression analysis of Hodgkin's disease (HD) lymph nodes was determined by comparing the conventional housekeeping genes, beta-actin, beta-tubulin, GAPDH, and the mouse gene LLRep3, that had been used previously in gene expression studies [5].

Psychiatry related information on Actb

• In order to furnish a combined model of relevance to human inclusion-body myopathy and Alzheimer's disease, transgenic mice expressing human betaAPP-C99 in skeletal muscle and brain under the control of the cytomegalovirus/beta-actin promoter were produced (Tg13592) [6].

High impact information on Actb

• The cardiac actin protein, normally found only in myofibrils, is stably accumulated at a high level, about one-third that of the endogenous mouse beta-actin [7].
• Using cloned cDNA probes for beta actin and alpha tubulin, we show that changes in mRNA activity correspond to a specific loss of these sequences during cellular differentiation [8].
• A primary response to many growth factor-induced transmembrane signals is the rapid activation of transcription of the proto-oncogene c-fos and other early-response genes, including the beta-actin gene [9].
• When mnt is expressed as a transgene under control of the beta-actin promoter in mice the transgenic embryos exhibit a delay in development and die during mid-gestation, when c- and N-Myc functions are critical [10].
• After beta-actin, the cytosolic brain isoform of creatine kinase was the next most abundant bundle protein; at approximately 0.5 mM, creatine kinase is capable of maintaining high ATP levels despite 1 mM/s ATP consumption by the plasma-membrane Ca(2+)-ATPase [11].

Chemical compound and disease context of Actb

• Northern blot analyses indicated that the treatment of PC12 cells with melatonin resulted in a significant decrease in the level of mRNA encoding beta APP, beta-actin, and glyceraldehyde-3-phosphate dehydrogenase, and that the treatment of a human neuroblastoma cell line with melatonin resulted in no change in levels of these messages [12].
• Murine erythroleukemia (MEL) cells exposed to DMSO were assessed for their ability to methylate poly(A)+ RNA and accumulate RNA transcripts of globin and nonglobin genes (c-myc, beta-actin and MER5) [13].
• Sarcomas arise when p53-deficient murine embryonic fibroblasts carrying beta-actin TVA and tet-o-K-ras4bG12D transgenes are infected with RCAS-rtTA-IRES-GFP and introduced into nude mice treated with the tet analog, doxycycline (dox); when dox is withdrawn, K-ras4bG12D levels fall, cells undergo apoptosis, and tumors regress [14].
• Pancreatic islet function and glucose homeostasis have been characterized in the transgenic YC-3.0 mouse, which expresses the yellow chameleon 3.0 (YC-3.0) protein under the control of the beta-actin and the cytomegalovirus promoters [15].

Biological context of Actb

• These CD-induced responses were reversible since recovering cells progressed through the G2 phase and resumed normal growth while beta-actin mRNA and protein synthesis rapidly returned to control levels [16].
• The rapid return of beta-actin mRNA to basal levels following CD removal did not require protein synthesis nor did it require progression through the G2 phase of the cell cycle [16].
• In contrast, transfection of another mutant form of the beta-actin gene which encodes an unstable protein had no impact on cell morphology or cytoarchitecture [17].
• The role of the beta-actin protein in generating the enlarged cell phenotype was examined by transfecting a mutant form of the human beta-actin gene [17].
• The gene coding for the cytoplasmic beta-actin is located on mouse chromosome 5 [18].

Anatomical context of Actb

• High level expression of the mutant beta-actin produced decreases in cell surface area and disruption of the actin microfilament network similar to that seen with transfection of the gamma-actin gene [17].
• The genes coding for the cardiac muscle actin, the skeletal muscle actin and the cytoplasmic beta-actin are located on three different mouse chromosomes [18].
• In late two-cell stage embryos, beta-actin, transferrin receptor and cyclin B mRNA levels were 10-20% of those in MII stage oocytes [19].
• Furthermore, no ODNs affected beta-actin mRNA and tumor necrosis factor alpha (TNF-alpha) expression in macrophages stimulated by LPS [20].
• Expression of GAPDH transcripts was less variable across tissues because this mRNA was only two-fold lower in liver as compared to either thymus or spleen, whereas expression of beta-actin transcripts was eight-fold lower in liver than in these tissues [21].

Associations of Actb with chemical compounds

• In one such resistant line, beta-actin was disrupted by viral insertion, and subsequent reconstitution of beta-actin expression levels in the mutant line Actin(mut) restored its sensitivity to TNF [22].
• Two protein synthesis inhibitors, cycloheximide and puromycin, blocked the CD-induced increase in beta-actin mRNA, in contrast to the serum-induced increase which is insensitive to inhibitors of protein synthesis [16].
• Transfectant C2 clones expressing high levels of human beta-actin displayed increases in cell surface area [17].
• According to the nucleotide sequencing analysis for one of the candidate clones, pMA 30, the predicted amino acid sequence was composed of 375 amino acids and was similar to that of beta-actin, but differed at the 28th amino acid in that leucine replaced the arginine of beta-actin [23].
• On the other hand, neither orchiectomy nor androgen treatment affected levels of mRNAs for EGFR in the kidney or mRNAs for the structural protein beta-actin in the liver [24].

Regulatory relationships of Actb

• Vectors containing the c-myc gene under control of the beta-actin gene promoter were transfected into M1 cells to obtain M1myc cell lines which constitutively synthesized c-myc [25].
• RESULTS: We demonstrate that a signaling pathway initiated by extracellular receptors acting through Rho GTPase and Rho-kinase regulates this spatial aspect of gene expression in fibroblasts by localizing beta-actin mRNA via actomyosin interactions [26].
• Upon differentiation, neuroblastoma cells reorganize their actin cytoskeleton and gamma actin is induced to polymerize whereas beta actin polymers are partially disassembled [27].
• Donor cells were dissected from beta-actin-enhanced green fluorescent protein (EGFP) transgenic mice and transplanted as a single cell suspension [28].
• In this study, we created CIS1 transgenic mice under the control of a beta-actin promoter [29].

Other interactions of Actb

• In contrast, myf5, beta-actin, UCP1 and glut1 mRNA levels gradually decreased during 8 days [30].
• However, mRNA expression of an early response gene, JunB, and constitutively expressed genes beta-actin and GAPDH were not inhibited by tyrphostin [31].
• Expression of beta-actin, however, was slightly increased in both rapidly growing and EGF-restimulated quiescent BALB/MK cells treated with TGF beta [32].
• In the studies reported here, it was found that inhibitors of polyamine biosynthesis, methylglyoxal-bis[quanylhydrazone] (MGBG) and difluoromethylornithine (DFMO), prevent mitogen-induced accumulation of mRNAs encoding major cytoskeletal components, beta-actin and alpha-tubulin, in mouse splenocytes [33].
• However, the mouse M1 progenitor myeloid cell line does not express RNA for IGF-I, as demonstrated by the absence of protected transcripts for IGF-I in the presence of abundant protected transcripts for beta-actin [21].

Analytical, diagnostic and therapeutic context of Actb

• Immunoprecipitation experiments show that DVL-1 coimmunprecipitates with spermatogenic cells beta-actin rather than alpha-tubulin [34].
• RT-PCR analysis demonstrated the presence of both beta-actin exon 1-hygromycin- and exon l-exon 2-containing transcripts in homozygous mutant embryos [35].
• Northern blotting showed that mRNAs for both beta-actin and vinculin were increased twofold in the overexpressing lines [36].
• By PCR, all organs with the exception of lung and brain showed low or undetectable expression of beta-actin [37].
• Myc protein expression, normalized to beta-actin expression, was measured by western blotting of tumor and splenic proteins [38].

References