BAG1 Mouse Monoclonal Antibody
- Known as:
- BAG1 Mouse Monoclonal Antibody
- Catalog number:
- APO-000573-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- BAG1 Mouse Monoclonal Antibody
Related genes to: BAG1 Mouse Monoclonal Antibody
- Gene:
- BAG1 NIH gene
- Name:
- BCL2 associated athanogene 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-19
- Date modifiied:
- 2016-10-05
Related products to: BAG1 Mouse Monoclonal Antibody
Related articles to: BAG1 Mouse Monoclonal Antibody
- The global impact of pulmonary tuberculosis (PTB) is compounded by a limited understanding of modifiable risk factors. While caffeine is the most consumed psychoactive substance, its causal relationship with PTB and the underlying immunological mechanisms remain unknown. - Source: PubMed
Publication date: 2026/04/20
Zhu LiangyuZheng ZidaHuang XunLu HaoranChen ZhiqiangWu HanxinPeng LiTao LvyanBai YueYang RuiBao RuianLuo SuyiMa WeijiangSong JieqinTang JiaomeiLi BingxueBao FukaiLiu Aihua - The BAG cochaperone 1 (BAG1) binds to oncogene BCL2 and markedly enhances its anti-apoptotic effects. This cochaperone represents a link between growth factor receptors and anti-apoptotic mechanisms mediated by endoplasmic reticulum stress. BAG1 interacts with the glucocorticoid receptor and modulates its transcription activity. As a cochaperone for several HSP70 proteins, it participates in control of protein folding. The present study aims to investigate the regulation of the BAG1 mRNA expression in U87MG glioblastoma cells by hypoxia and glucose or glutamine deprivation, depending on the inhibition of ERN1 (endoplasmic reticulum to nucleus signaling 1) with the intent to reveal the role of ERN1 signaling in the regulation of this gene expression and function in oncogenesis. The U87MG glioblastoma cells (transfected by an empty vector; control) and cells with inhibited ERN1 endoribonuclease and protein kinase (dnERN1) or only ERN1 endoribonuclease (dnrERN1) were used. Silencing of ERN1 and XBP1 mRNAs for suppression of ERN1 function was also used. A hypoxic condition was created by dimethyloxalylglycine (4 h). DMEM medium without glucose or glutamine was used for glucose and glutamine deprivation (16 h). The expression level of the BAG1 mRNA was studied by real-time qPCR and normalized to the beta-actin mRNA. Inhibition of the endoribonuclease activity of ERN1 significantly decreased BAG1 mRNA expression. However, a lesser suppression of this mRNA expression was observed in dnERN1 cells (with inhibited ERN1 endoribonuclease and protein kinase) indicating the involvement of protein kinase in controlling BAG1 expression. The silencing of ERN1 and XBP1 mRNAs also reduced the expression of BAG1 mRNA demonstrating the involvement of XBP1s in this regulation. The expression of the gene was resistant to glutamine deprivation and upregulated in response to glucose deprivation in control glioblastoma cells. However, the inhibition of ERN1 increased the sensitivity of gene expression to both glucose and glutamine deprivation. Furthermore, the expression of the gene was increased under hypoxia in control U87MG cells; however, a greater induction was observed in dnERN1 cells. The results of this study demonstrated that ERN1 inhibition reduces BAG1 mRNA expression through the endoribonuclease activity of ERN1 and that protein kinase activity counteracts endoribonuclease in regulating the expression of BAG1 mRNA. Moreover, ERN1 inhibition also enhances the sensitivity of BAG1 mRNA expression to nutrient supply and hypoxia resulting in reduced resistance of glioblastoma cells. - Source: PubMed
Publication date: 2026/03/24
Viletska Yuliia MMinchenko Oleksandr HKhita Olena OTsymbal Daria OSliusar Myroslava YHalkin Oleh VKozynkevych Halyna EMinchenko Dmytro O - Diquat is a widely used bipyridyl herbicide, and central nervous system injury (CNSI) is a major cause of death in acute poisoning; early serum markers and underlying mechanisms remain unclear. We prospectively classified acutely poisoned patients into healthy controls (JKDZ), diquat patients without CNSI (NCNSI), patients who developed CNSI during hospitalization (CNSI1), and patients presenting with CNSI (CNSI2). Early serum underwent transcriptomic, proteomic and metabolomic profiling. Multivariate and differential analyses with KEGG/GO enrichment and O2PLS integration identified key pathways and candidate markers, which were evaluated by violin plots and ROC curves. Mechanistic relevance was tested in zebrafish embryos exposed to diquat (Control, 100, 175 mg/L) by assessing developmental toxicity, locomotor behavior and neuroinflammation-related gene expression. Integrated multi-omics clearly separated the four clinical groups and revealed progressive disruption of glycolysis/gluconeogenesis, central carbon and amino-acid metabolism, serotonergic synapse and ferroptosis pathways with increasing CNSI. Integration pointed to early l-histidine depletion, mitochondrial dysfunction and accumulation of the neurotoxic metabolite methylmalonate. Serum 5-hydroxyindoleacetic acid (5-HIAA), BAG1 and CLIC1 strongly discriminated NCNSI from CNSI1/2 (AUC 0.94-1.00). In zebrafish, diquat caused microphthalmia and other malformations, reduced swimming distance and speed, and robust induction of cxclc1c, ifna6, mmp9 and tnfa. In zebrafish, targeted absolute quantification confirmed a dose-dependent decrease in l-histidine and increases in MMA and 5-HIAA following diquat exposure. Clinical multi-omics combined with zebrafish evidence suggests an association between diquat exposure, histidine depletion, mitochondrial stress and methylmalonate accumulation, accompanied by neuroinflammation and CNSI. Serum 5-HIAA, BAG1 and CLIC1 are promising early-warning biomarkers for CNS complications in diquat poisoning. - Source: PubMed
Publication date: 2026/03/20
Liu QiqiLi JiaweiMeng YunlongXiong GuanghuaYan MinLv TingzhanLiu HongboYang Yihong - Toxoplasmosis is a major foodborne zoonosis causing high global disease burden and economic losses in sheep and goat industries. The gold standard for detecting viable Toxoplasma gondii is the mouse bioassay, which involves inoculating tissues from infected animals into laboratory mice. Here, we describe a faster, cost-effective, and ethical alternative method to assess T. gondii presence and viability. The procedure is based on reverse transcription quantitative PCR (RT-qPCR) targeting messenger RNA transcripts of genes highly expressed during infection, including the bradyzoite-specific gene bag1, indicative of chronic infection and gra1, which detects both acute and chronic infections due to high transcription in tachyzoites and bradyzoites. This RT-qPCR assay was evaluated alongside the mouse bioassay and two molecular methods, 529 bp-specific qPCR and nested ITS-1 PCR, using tissues from experimentally infected piglets and sheep. Cohen's kappa coefficient showed moderate agreement between gra1-bag1 RT-qPCR and the mouse bioassay (κ = 0.557), comparable to 529-qPCR (κ = 0.556). The assay detected gra1 and bag1 transcripts in all bioassay-positive samples, demonstrating high predictive value for viable parasites. The gra1-bag1 RT-qPCR provides a reliable prescreening tool for predicting parasite viability in tissues, supporting ethical research by reducing reliance on the mouse bioassay. - Source: PubMed
Publication date: 2026/03/21
Largo-de la Torre AndreaVelasco-Jiménez NataliaOrtega-Mora Luis MiguelRegidor-Cerrillo Javier - Often, more pollen grains land on recipient flowers than there are ovules to fertilize. Consequently, the haploid male gametophyte engages in post-pollination competition, one way that pollen genotype can influence inheritance. The maize (Zea mays subsp. mays L.) inflorescence (ear), with its elongated stigma and style structures (silks), has a conspicuous spatial heterogeneity, with longer silks at the base of the ear than at the apex. To evaluate the hypothesis that alleles with reduced pollen fitness influence the spatial distribution of progeny genotypes along the ear, we developed an updated phenotyping platform that maps fluorescently marked mutant (Ds-GFP) kernel phenotypes on the ear via an implementation of the Faster R-CNN machine vision model (EarVision.v2) and a statistical pipeline that evaluates the relationship between kernel position and transmission ratio (EarScape). Our dataset (1384 ears) represents 58 Ds-GFP insertion alleles. None of the 48 alleles with Mendelian inheritance showed any significant spatial trend. In contrast, 50% of alleles with a pollen-specific transmission defect (5/10) exhibited significant spatial effects. An insertional mutant of the gene encoding a putative actin-binding protein, base-to-apex gradient1* (bag1*), is associated with decreased mutant transmission at the ear base relative to the apex. Surprisingly, a mutant allele of another pollen-expressed gene (Zm00001eb236740) generates the opposite trend, decreased mutant transmission toward the ear apex; and two mutant alleles of the sperm cell attachment factor gamete expressed2 (gex2) can produce ears with transmission highest at both base and apex. We conclude that pollen fitness mutants cause unexpectedly diverse spatial patterns of progeny genotypes. - Source: PubMed
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