HSPA6 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- HSPA6 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100154
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- HSPA6 antibody Polyclonal Antibodies Primary antibodies
Related genes to: HSPA6 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- HSPA6 NIH gene
- Name:
- heat shock protein family A (Hsp70) member 6
- Previous symbol:
- -
- Synonyms:
- HSP70B'
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-26
- Date modifiied:
- 2015-11-19
Related products to: HSPA6 antibody Polyclonal Antibodies Primary antibodies
Related articles to: HSPA6 antibody Polyclonal Antibodies Primary antibodies
- Glioblastoma multiforme is an aggressive and therapy-resistant tumor, necessitating the identification of novel therapeutic targets. Here, we investigated the role of transient receptor potential vanilloid 1 (TRPV1) in mediating capsaicin-induced changes in cell viability in U87 glioblastoma cells. Wild-type cells tolerated capsaicin concentrations up to 175 μM, whereas TRPV1 knockout (TRPV1KO) cells exhibited reduced viability at 164 μM, indicating a cytoprotective function of TRPV1. Transcriptomic analyses revealed that wild-type cells activated the MAPK-MSTRG.66879-MYC-HSF1-axis, resulting in robust induction of heat shock proteins (HSPA1B, HSPA6, HSP90AA1) and dual-specificity phosphatases (DUSP1, DUSP8, DUSP10), which collectively maintained protein homeostasis and mitigated cellular damage. In contrast, TRPV1KO cells displayed impaired calcium-mediated MAPK activation, leading to altered mitochondrial oxidative phosphorylation, significant changes in electron transport chain (ETC I, II, III, IV), and enhanced intrinsic apoptosis through HRK. Notably, two long non-coding RNAs, MSTRG.56099 and MSTRG.66879, were identified as potential cis-regulators of DUSP1 and MYC, respectively. MSTRG.66879, upregulated in wild-type cells, appeared to form a TRPV1-associated regulatory axis with MYC and miR-182, promoting cell survival under capsaicin exposure. Disruption of this network in TRPV1KO cells sensitized them to capsaicin-induced apoptosis. Collectively, TRPV1 orchestrates calcium influx, MAPK signaling, heat shock protein induction, and noncoding RNA-mediated regulation to facilitate glioblastoma cell adaptation, suggesting that targeting TRPV1 and the MSTRG.66879-MYC axis may offer new therapeutic avenues and biomarkers for glioblastoma management. - Source: PubMed
Publication date: 2026/04/10
Chinreddy Subramanyam ReddyMashozhera Nicole TendayiLee GwonjinZaman IqraaPatel VaibhaviHarris Robert THankins Gerald RReddy Umesh K - Immune thrombocytopenia (ITP) is a hematological disorder commonly found in individuals of any gender, race, or age. Patients with ITP will present with thrombocytopenia either in a primary form or because of an infection or a dysfunction in the immune system. The severity of ITP is linked to diminished production of platelets due to the blockage of production in the bone marrow niche and increased destruction of platelets, which confirms the diagnosis of the disorder. The investigation of the pathogenesis of ITP is of critical importance as it can give an important indication of the state of the patient, guiding us through risk assessment and treatment. Proteomics can provide tools to explore the protein profile of ITP. In this review, we aimed to uncover different biomarkers, both diagnostic and prognostic, that have been investigated with proteomic methodologies and that might help in understanding the pathogenesis of ITP and providing personalized treatment to patients. Several differentially abundant proteins were identified, including haptoglobin isoforms, heat shock proteins (HSPA6, HSPA8), integrin β3 (ITGB3), 14-3-3 protein eta (YWHAH), vitamin D-binding protein, fibrinogen chains, MYH9, and FETUB, which are involved in key signaling pathways, such as PI3K/akt, TNF-a, and mTOR, and they demonstrate potential as diagnostic and prognostic biomarkers. Collectively, current data support the value of proteomics for uncovering the molecular landscape of ITP and guiding the development of precision diagnostics and personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/03/12
Boura-Theodorou AnastasiaPsatha KonstantinaManiatsi StefaniaKourti AretiKaiafa GeorgiaAivaliotis MichalisMakedou Kali - Myocardial infarction (MI) is a myocardial necrosis event caused by an unstable ischemic state that reduces life expectancy primarily through cardiac functional impairment and cardiomyocyte death. The present study aims to investigate the genetic mechanisms underlying MI by integrating expression quantitative trait loci (eQTLs) and Mendelian randomization (MR) analyses. - Source: PubMed
Publication date: 2026/03/11
He PeichunLv XiangwenFu ChuwenQin ZhenChen SiyuanZhao JinminXie Jian - Recent mpox outbreaks have shown a predominant transmission through sexual contact. Replication-competent virus has been detected in seminal fluid, while in female patients, vaginal lesions, vertical transmission, and miscarriage risk have been reported. This study explored the susceptibility of the lower female genital tract (LFGT) to monkeypox virus (MPXV) infection, the role of sex-hormones in modulating viral replication, and host-virus molecular interactions. Human vaginal (VK2/E6E7) and ectocervical (Ect1/E6E7) epithelial cells were exposed to MPXV clade IIb, and viral replication was assessed. The influence of sex-hormones was evaluated after pretreatment with physiological concentrations of 17-β-estradiol or progesterone. Cellular genes' expression was determined by RT-qPCR and RNAseq, and ELISA was used for protein release analysis. Both cell lines supported productive MPXV infection. 17-β -estradiol and progesterone slightly reduced viral replication in Ect1/E6E7. At 48 hours post-infection, compared to uninfected control, 216 differentially expressed genes (DEGs) were identified in MPXV infected VK2/E6E7 and 11 in Ect1/E6E7, with nine shared DEGs involved in protein folding (HSPA6), chemotaxis (CXCL3, ARC), inflammation and lymphoproliferation (IL11, IL1RL1, MMP-1), and tissue remodeling (IGFN1, MMP-1). MPXV infection significantly increased MMP-1 release in both cell lines, and MMP-1 inhibitors reduced infectious virus production. IFN-β and IFN-λ1 were induced earlier and more pronouncedly in Ect1/E6E7 which also showed slower viral replication than VK2/E6E7. Our analysis demonstrated the MPXV-mediated modulation of common and tissue-specific cellular pathways in the LFGT. The perturbation of tissue remodeling and inflammation in this district has the potential to affect reproductive health and susceptibility to sexually-transmitted-infections. - Source: PubMed
Publication date: 2026/03/29
Mariotti DavidePicarone LudovicaD'Auria AlessandraRosa LuigiValeriani ValentinaPietrucci DanieleMeschi SilviaCarletti FabrizioMazzotta ValentinaAntonelli GuidoGirardi EnricoScagnolari CarolinaChillemi GiovanniAntinori AndreaMaggi FabrizioMatusali Giulia - The molecular mechanisms underlying adaptation to physical exertion and racing stress in horses remain incompletely understood. Peripheral blood transcriptomics offers a minimally invasive method to monitor systemic responses to exercise and identify biomarkers of adaptation or overload. - Source: PubMed
Publication date: 2026/03/07
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