HSPA1B Mouse Monoclonal Antibody
- Known as:
- HSPA1B Mouse Monoclonal Antibody
- Catalog number:
- BIN-003304-M05
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- HSPA1B Mouse Monoclonal Antibody
Related genes to: HSPA1B Mouse Monoclonal Antibody
- Gene:
- HSPA1B NIH gene
- Name:
- heat shock protein family A (Hsp70) member 1B
- Previous symbol:
- -
- Synonyms:
- HSP70-2
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-11
- Date modifiied:
- 2016-10-05
Related products to: HSPA1B Mouse Monoclonal Antibody
Related articles to: HSPA1B Mouse Monoclonal Antibody
- Chronic stress significantly impacts hippocampal function through transcriptional and epigenetic mechanisms. While the roles of lncRNAs in stress-related transcriptional and epigenetic regulation have recently been recognized, their genome-wide functions controlling the transcriptional network remain largely unclear. Evidence indicates that the lncRNA uc.104 is involved in stress responses; however, its genome-wide chromatin interactions and gene regulatory effects are yet to be explored. To examine this, we combined chromatin isolation by RNA purification sequencing (ChIRP-seq) and RNA sequencing (RNA-seq) in the hippocampus from handled control and chronic restraint stress (CRS) rats. ChIRP-seq identified 6,664 uc.104 binding peaks under CRS, including 6,517 enriched and 149 reduced. Many peaks were mapped to intronic and promoter-proximal regions of protein-coding genes. Integration of ChIRP-seq with RNA-seq data revealed 1,839 differentially expressed genes associated with uc.104 binding sites, with 106 high-confidence overlaps. Several genes (Gabra3, Htr7, Irs1, Gpr37, Clu, Hspa1b, Ppp3r2, Nfasc, Pcdhac2, and Cysltr2) identified as regulatory targets of uc.104, have been directly implicated in stress responses, synaptic plasticity, and neuroinflammation. Gene ontology and Synapse GO (SynGO) analyses revealed significant enrichment for processes involving dendritic spine formation, synapse organization, and pre- and postsynaptic signaling. Protein-protein interaction analysis identified hub genes, including EGFR, CDC42, IGF1R, CTNNB1, CALM1, CALM3, POLR2A, MDM2, TBP, and CSNK1E, several of which have been linked to stress-responsive pathways. Together, our findings reveal that uc.104 binding to chromatin near stress- and synapse-related genes may act as a regulator of stress-responsive transcriptional networks in the hippocampus. By linking uc.104 occupancy to stress and synaptic responsive genes, this study highlights uc.104 as a potential mediator of stress-induced hippocampal malfunctions. - Source: PubMed
Publication date: 2026/04/19
Verma Anuj KRoy BhaskarPrall KevinHulwi EllieDwivedi Yogesh - This study employed an integrative bioinformatics approach to identify key molecular signatures in Parkinson's disease (PD) by analyzing substantia nigra transcriptomes from 22 PD patients and 22 healthy controls (HCs) across three Gene Expression Omnibus (GEO) datasets. Using DESeq2, edgeR, and limma, we identified 85 consensuses differentially expressed mRNA (DEmRNAs) (23 up-regulated and 62 down-regulated), including key players in PD pathogenesis such as molecular chaperones (DNAJB1, HSPA1B/L), dopaminergic markers (TH, SLC6A3), and extracellular matrix components (COL5A1, LAMB1). Functional enrichment analyses revealed up-regulated pathways in PI3K-Akt signaling and extracellular matrix organization, while down-regulated genes were enriched in dopaminergic synapse and mitochondrial function pathways. Protein-protein interaction (PPI) network analysis identified 20 hub genes, with DNAJB1, TH, KCNJ6, and SLC6A3 emerging as central regulators. Notably, we discovered novel candidate's mRNAs alongside validated PD-associated genes, highlighting both degenerative processes and compensatory mechanisms. These findings provide a comprehensive molecular framework for PD pathogenesis, offering potential biomarkers and therapeutic targets for further investigation. - Source: PubMed
Publication date: 2026/04/13
Aung Tun LinAung Ye WinMyint Khin SandiShi Xiaoran - To explore the regulatory aspects of mRNAs and miRNAs in suicide, we integrated transcriptomic data from GEO datasets. The analysis of mRNA expression in the prefrontal cortex of suicide victims with major depressive disorder revealed a differential profile with 27 downregulated mRNAs, including , , , , and , which are involved in proteostasis, transcriptional regulation, and apoptosis. Functional enrichment analysis using KEGG and Gene Ontology (GO) revealed significant associations with synaptic plasticity, neuronal survival, and signaling pathways, including MAPK, TGF-β, Wnt, p53, and neurotrophins. Subsequently, using the GSE34120 GEO dataset of miRNAs from the frontal cortex of suicide victims, 105 dysregulated miRNAs were identified. The networks revealed compact regulatory modules with hsa-miR-576-3p, hsa-miR-493, and hsa-miR-550, as well as highly connected central nodes such as hsa-miR-30b, hsa-miR-16a-5p, hsa-miR-181a-5p, and hsa-miR-184. The integration of both profiles allowed the elaboration of miRNA-mRNA regulatory networks in which , , , and interact with multiple dysregulated miRNAs. These findings support the notion that suicide involves complex post-transcriptional dysregulation, particularly related to astrocytic function and neurotrophic signaling, with potential diagnostic and therapeutic applications. - Source: PubMed
Publication date: 2026/03/30
Cortéz-Sánchez José LuisRivera-Escobar Hernán MauricioMuñoz Roa Esther NataliaZabala-Bello Carlos AndrésPérez-Sánchez GilbertoChin Chan José MiguelBautista-Ortiz MonserratLópez-Martínez Karla MaríaOsorio-Antonio FedericoGálvez-Romero José LuisCarrasco Carballo AlanSedeño-Monge VirginiaCastelán FranciscoBautista-Rodríguez Elizabeth - 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 - FLT3-ITD inhibitors are approved for acute myeloid leukemia (AML) treatment but relapse is common. In this study, the combined inhibition of FLT3-ITD signal and protein translation by QUIZartinib and Omacetaxine Mepesuccinate (QUIZOM) synergistically suppressed the most critical FLT3-ITD survival signals including mitochondrial respiration and proteostasis, which induced apoptosis and pro-inflammatory response. In a Phase 2 trial (NCT03135054) involving 40 chemo-refractory/unfit FLT3-ITD AML patients, QUIZOM achieved a composite complete remission (CRc) of 83%, a median leukemia-free survival (LFS) of 10 months (Range: 0.7-68.2 months) and a median overall survival (OS) of 12.9 months (Range: 1.8-69.2 months). 13/33 (39%) received allogeneic HSCT after a median of 143 days (Range: 53-367 days). Higher CRc rates were observed in patients with NPM1 mutations, DNMT3A mutations, and wild-type WT1. Single-cell RNA-sequencing of QUIZOM cohort revealed positive correlation between pro-inflammatory response in blasts, CD8 + T activation and clinical responsiveness. Further, we identified a leukemic stem cell (LSC) subpopulation with activated JNK/JUN/HSPA1B axis via PLD1-driven phosphatidylcholine metabolism, which promoted proteostasis and drove QUIZOM resistance. PLD1-inhibitor remodeled phospholipid metabolism, induced ferroptosis and restored QUIZOM response in LSC. Our findings provided the therapeutic and resistant mechanisms of QUIZOM and paved the way for targeted interventions in this AML subtype. - Source: PubMed
Publication date: 2026/04/06
Zheng Li-ChuanWong Kelvin K WLam Stephen S YLeung Garret M KLi ChenqinyaoTong Kwui-WaLam WingZeng Xiao-YuanChan Koon-ChuenChan Natalie Nok-ManNg Ka-LamDang Chee-CheanKwok Tsz-HoTsui Sze-PuiSharma RakeshWong Jason W HLeung Suet-YiLeung Anskar Y HMan Cheuk-Him