Ask about this productRelated genes to: HSPA6 antibody
- 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
Related articles to: HSPA6 antibody
- Heat shock proteins of the HSP70 family and their BAG co-chaperones regulate responses to oxidative stress, inflammation, apoptosis, and ischemia, all central to coronary artery disease (CAD) pathogenesis. The contribution of genetic variants within HSP70-family and BAG co-chaperone genes to CAD susceptibility remains unclear. Thus, we sought to evaluate associations of HSP70- and BAG-related SNPs with CAD risk and to characterize their potential regulatory effects using comprehensive bioinformatic analyses. A case-control cohort of 834 CAD patients and 1328 controls of Russian ethnicity was genotyped for 13 SNPs. Associations with CAD susceptibility and traits were tested using log-additive regression with adaptive permutation. Loci underwent functional annotation. The C allele of BAG1 rs706121 was associated with increased CAD risk overall (OR = 1.24, p = 0.019), in males (OR = 1.39, p = 0.002), and in smokers (OR = 1.39, p = 0.020). BAG3 rs196329 was associated with lower risk in males (A allele: OR = 0.82, p = 0.040), whereas HSPA6 rs753856 was associated with reduced risk in physically active individuals (G allele: OR = 0.61, p = 0.008). Additional associations involved clinical or biochemical traits. Functional annotation identified potential regulatory effects, including eQTL associations, overlap with histone marks, and allele-dependent changes in transcription factor binding. HSP70 and BAG variants may contribute to CAD susceptibility and support sex- and lifestyle-informed risk assessment. - Source: PubMed
Publication date: 2026/08/15
Polshvedkina OlgaKobzeva KseniaOrlov Yuriy LBushueva Olga - Endometriosis is a chronic, oestrogen-responsive inflammatory disease characterised by endometrial-like tissue outside the uterine cavity. Because retrograde menstruation is common, lesion establishment probably requires cellular competence and a permissive ectopic microenvironment. This hypothesis-driven narrative review evaluates fascin () as a candidate cytoskeletal effector and considers antecedent eutopic priming versus induction after ectopic adhesion. Functional evidence was integrated with a targeted public-data screen. Donor-level reanalysis of GSE179640 found no conclusive overall eutopic case-control difference and predominantly non-epithelial expression. Exploratory analysis of GSE203191 suggested higher expression within a + stromal subcluster in diagnosed cases, without a comparable epithelial signal or detectable increase in subcluster abundance. This small post hoc analysis remains hypothesis-generating. was absent from the published HECA stromal/macrophage differential-expression lists and was not prioritised by the 2023 endometriosis GWAS. The current evidence therefore argues against uniform epithelial or whole-eutopic overexpression but permits a lineage-restricted stromal state. Fascin participates in autophagy- and miR-145-sensitive invasion networks, although these pathways are pleiotropic. Validation requires cycle- and lineage-resolved tissue mapping, compositional controls, matched lesions, and direct perturbation. Fascin should currently be regarded as a candidate multi-marker component and preclinical target, not a validated biomarker or systemic therapeutic target. - Source: PubMed
Publication date: 2026/08/13
Marín-Sánchez María PilarOrtega-Suárez DaimarisLópez-Soto Álvaro FedericoKozak IrynaBenito-Villena RebecaVives-Ramírez MarinaPostigo-Corrales FátimaIsaac-Montero AlejandraConesa-Zamora PabloLuengo-Gil Ginés - Hsp70 chaperones are central regulators of proteostasis, mediating folding, refolding, degradation, and aggregation-prevention. Their activity is tuned by the diverse J-domain proteins (JDPs), which both recruit client proteins and stimulate Hsp70 ATP hydrolysis via interaction with a conserved J-domain. The cytosol contains four Hsp70 paralogs-the stress-inducible HSPA1A/B and HSPA6, and the constitutively expressed HSPA8. Whether these act redundantly or carry distinct cellular functions has remained unresolved. Here, we systematically map the interactions of cytosolic Hsp70s with broad-specificity JDPs to elucidate how paralog identity shapes cellular function. We found that despite the high conservation of the JDP-Hsp70 interaction sites, the affinities of these interactions and their functionality varied greatly. HSPA8 behaves as a generalist, engaging all JDP classes with comparable affinity, consistent with its housekeeping role. By contrast, HSPA1 preferentially binds canonical Class A and B JDPs, while showing only weak binding to Class B'. Therefore, under stress, HSPA1 pairs only with Class A/B JDPs to support robust protein refolding, while freeing Class B' to suppress protein aggregation in an Hsp70-independent manner. Most unexpectedly, HSPA6, the most stress-inducible paralog, binds selectivity to Class B JDPs, losing interactions with both Class A and B'. Thus, under severe stress, HSPA6 works exclusively with Class B JDPs to ensure ATP-dependent protein repair, while freeing Class A and B' JDPs to act independently of Hsp70 to protect damaged/misfolded proteins. Our findings reveal an evolved hierarchy of paralog-specific JDP couplings that dynamically rewires the Hsp70 network from active repair to protection during stress. - Source: PubMed
Publication date: 2026/08/18
Suhler Ronivan Beurden Lars J WShmueli Merav DFaust OfrahRosenzweig Rina - Cervical cancer (CC) is a prevalent malignancy in women. RNA-binding motif single-stranded interacting protein 3 (RBMS3) acts as a tumor suppressor in many cancer types, but its role and underlying regulatory mechanisms in CC remain unclear. - Source: PubMed
Huang HuapingLi PingZhu LixiaWu YaweiLiu QinZhang Hong - Ovarian cancer (OC) persists as a highly fatal gynecologic tumor, underscoring the urgent need for dependable diagnostic markers and innovative therapeutic strategies. In this study, we identify Arachidonate 12-lipoxygenase (ALOX12) as a previously unrecognized ferroptosis-related tumor suppressive regulator with significant diagnostic and prognostic value in OC. By integrating Weighted Gene Co-expression Network Analysis (WGCNA), machine learning algorithms, and survival modeling, and validating our findings through in vitro and in vivo experiments, transcriptomic profiling, and biochemical assays, we systematically characterized the biological and mechanistic roles of ALOX12. Our analysis revealed that ALOX12 is markedly downregulated in OC tissues, with its low expression correlating with poor clinical outcomes. Functional experiments further demonstrated that ALOX12 suppresses OC cell proliferation, invasion, and migration, while promoting apoptosis and ferroptosis-associated lipid peroxidation. Mechanistically, transcriptome sequencing and protein assays pinpointed MAPK signaling as a key pathway modulated by ALOX12. Additionally, our experiments revealed that ALOX12 exerts its effects by regulating HSPA6 expression. Collectively, these findings highlight ALOX12 as a promising biomarker and potential therapeutic target, offering new insights into ferroptosis-associated signaling networks and their implications for improving the management of OC. - Source: PubMed
Publication date: 2026/07/24
Fang YihuaLiu XueningYang MengyaoZhang XiaohuiLi MinCao Yunxia