Ask about this productRelated genes to: HSPA1L Blocking Peptide
- Gene:
- HSPA1L NIH gene
- Name:
- heat shock protein family A (Hsp70) member 1 like
- Previous symbol:
- -
- Synonyms:
- HSP70-HOM, hum70t
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-12
- Date modifiied:
- 2016-10-05
Related products to: HSPA1L Blocking Peptide
Related articles to: HSPA1L Blocking Peptide
- Acute pancreatitis (AP) is a painful and potentially life-threatening disorder, with no effective therapy available to date. Genome assessment shows promise as a potential method for predicting AP severity. We hypothesized that single nucleotide polymorphisms (SNPs) and expression changes in Heat Shock Protein 70 (HSP70) family genes may play a role in early prediction of AP severity. - Source: PubMed
Publication date: 2026/09/01
Kielaite-Gulla AisteGaizevska JustinaSestokaite AgneSabaliauskaite RasaSnipaitiene KristinaJarmalaite SonataDamaseviciute RyteStrupas Kestutis - : The genes encoding , , and , located in the MHC class III region at 6p21.3-22.1, a region implicated in susceptibility to schizophrenia, are critical regulators of neurodevelopmental processes and contribute to synaptic neuroprotection. This study investigated whether the , , and genes are associated with schizophrenia. : We sequenced the coding regions of , , and from 100 patients with schizophrenia to identify genetic variants. Further, we conducted a genetic association analysis of three SNPs (rs9469057, rs142416335, and rs2075800) in the gene in 519 patients with schizophrenia and 1492 healthy controls from the Taiwan Biobank. We analyzed the function of the HSPA1L protein via immunoblotting. : We identified 17 coding variants, including 8 missense and 9 synonymous mutations, in 100 patients with schizophrenia. Three variants (, , and ) in the gene did not exhibit any significant differences in allele or genotype frequencies between patients and control subjects. Notably, one ultra-rare missense mutation, , was not documented in the control sample in Taiwan BioBank. Immunoblotting revealed mutant with decreased protein expression in SH-SY5Y cells compared with the wild type. : While common variants in the , , and genes do not seem to be significant genetic risk factors for schizophrenia in this cohort, the ultra-rare mutation, , significantly reduces protein expression. These preliminary findings suggest that a potential loss-of-function or reduced expression of the gene may be a predisposing factor contributing to schizophrenia vulnerability in certain individuals. However, the finding should be replicated in other independent samples. The in vitro and in vivo impacts of the associated mutation at the gene on the pathophysiology of schizophrenia are worthy of future investigation. - Source: PubMed
Publication date: 2026/06/23
Wang Ying-ChiehHsu Shih-HsinTsai Hsin-YaoCheng Min-Chih - Diabetic nephropathy (DN) is the most common complication of diabetes, with immune-mediated inflammation playing a significant role in its pathophysiology. The complement system, a key proinflammatory factor, is implicated in DN. This study was aimed at identifying diagnostic biomarkers related to the complement system in DN using bioinformatics methods. We analyzed three datasets (GSE96804, GSE104948, and GSE1009) from public databases, employing differential expression analysis and machine learning to identify complement system-related genes (CSRGs) as potential biomarkers. A diagnostic nomogram was constructed based on these genes, and immune microenvironment differences between the DN and control groups were explored. Gene interaction networks, enrichment analysis, and drug predictions were also conducted. Mendelian randomization (MR) was used to examine the causal links between identified biomarkers and DN. Our analysis identified five biomarkers (CKB, ANXA1, HSPA1L, CYP27B1, and XYLT1) associated with DN. A diagnostic nomogram based on these biomarkers showed high accuracy (model correction slope close to 1 and AUC close to 1). Immune infiltration analysis revealed significant differences in immune cell subsets between the DN and control groups. Gene set variation analysis (GSVA) indicated that the oxidative phosphorylation (OXPHOS) pathway was activated in CKB, HSPA1L, CYP27B1, and XYLT1 while inhibited in ANXA1. MR confirmed HSPA1L as a risk factor for DN (OR = 1.625, 95% CI: 1.272-2.076, p = 9.96e - 05). In conclusion, these five CSRGs may play significant roles in DN progression, providing a foundation for further research into DN pathogenesis and potential molecular markers for clinical diagnosis. - Source: PubMed
Wei LifangLi YeLu YuhuiXu MinminYu YueLi LijieLin MinFan LifeiCai Jing - Alzheimer's disease (AD) is a progressive disorder characterized by cognitive decline. Physical exercise and audiovisual stimulation have gained increasing concern for their potential to mitigate AD pathology. However, the therapeutic advantages of combining these interventions and the precise molecular mechanisms underlying these strategies need further demonstration. - Source: PubMed
Publication date: 2026/05/29
Jia JunXie GuominZheng WuXu ChunshuangXia YuxinHu QiaoxiaXiang BinbinZhou XinkaiChen AnqiChen XiaopingWang QinwenZhou YingsongXu Shujun - Photoaging is an extrinsic skin aging process caused by chronic ultraviolet (UV) radiation. A core pathological feature of photoaging is excessive oxidative stress, which can further induce ferroptosis. The HSP70 family plays a critical role in this stress response by protecting the key antioxidant enzyme GPX4. In this study, we established UV-induced photoaging models in cultured cells and 3D skin organoids. UPLC-MS/MS analysis of Chenpi transdermal permeate (prepared by in vitro transdermal penetration of Chenpi extract through mouse skin) identified hesperidin as the primary bioactive compound of Chenpi (dried peel of the plant Blanco after the aging process). The efficacy of hesperidin was validated in human keratinocytes (HaCaTs), fibroblasts (HSFs), and skin organoids. Mechanistically, transcriptomic and metabolomics analysis indicated that ferroptosis is a key pathway through which hesperidin ameliorates photoaging. Limited proteolysis mass spectrometry (LiP-MS), transcriptomics, and molecular dynamics simulation results demonstrated that hesperidin directly binds to the molecular chaperone HSPA1L. By upregulating HSPA1L expression, hesperidin enhanced the stability of GPX4 and suppressed UV-triggered ferroptosis. Our findings identify the HSPA1L/GPX4 axis as a critical redox regulatory pathway targeted by hesperidin, providing a mechanistic foundation for anti-photoaging therapies. - Source: PubMed
Publication date: 2026/04/14
Guo XiaoyuWu MengyaoLi YunxingHe JianlangMa YongjieSu TaizhiLi ChangzhengWang Jian