Ask about this productRelated genes to: HSBP1 protein
- Gene:
- HSBP1 NIH gene
- Name:
- heat shock factor binding protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-30
- Date modifiied:
- 2014-11-19
Related products to: HSBP1 protein
Related articles to: HSBP1 protein
- The cerebellar cortex presents a repetitive structure, but the main projecting neurons of this tissue, the Purkinje cells, are not identical and behave differently to various types of injury. Common patterns of neurodegeneration exist, where certain Purkinje cells die earlier than others. By contrast, lobe X of the cerebellum is a particularly resistant structure, independently of the cerebellar disease or damage. However, the mechanisms underlying the survival capability of these especially resistant Purkinje cells are still unknown. In this work, we have used the Purkinje Cell Degeneration (PCD) mouse, a model of severe cerebellar degeneration that also reproduces the human disease called childhood-onset neurodegeneration with cerebellar atrophy, to study Purkinje cell resistance. After an exhaustive immunochemical analysis of the different subpopulations of Purkinje cells, the Heat Shock Protein 25 (HSP25) and its phosphorylated version HSP25-P-Ser15 were found to be especially induced in lobe X of PCD mice. As this protein has neuroprotective properties, it may be responsible for resistance against cerebellar neurodegeneration. Taking into account the constant resistance of lobe X, the use of HSP25 may lead to new possibilities for achieving natural protection both in cerebellum and in other brain structures, or even for developing future neuroprotective therapies. - Source: PubMed
Publication date: 2026/01/23
Hernández-Pérez CarlosPérez-Revuelta LauraTéllez de Meneses Pablo GCabedo Valeria LAlonso José RamónDíaz DavidWeruaga Eduardo - The Nonalcoholic fatty liver disease (NAFLD) is a major chronic liver condition, with its pathology remaining elusive. Consequently, a thorough exploration of the underlying mechanisms driving NAFLD progression is essential for a comprehensive understanding of this metabolism-associated disorder. - Source: PubMed
Publication date: 2026/02/02
Zhang XuechunCheng YingYu RunzhiHu XiaonaHuang Yiqin - Colorectal cancer (CRC) ranks as the third most common cancer globally and is characterized by a poor prognosis. Abnormal glycosylation, a hallmark of cancer development, influences multiple signaling pathways and contributes to CRC progression. Identifying key glycosyltransferase genes associated with CRC prognosis could provide novel therapeutic targets and improve patient outcomes. We utilized datasets from The Cancer Genome Atlas (TCGA) to analyze the expression of glycosyltransferase genes in CRC tissues. Lasso regression and COX regression models were employed to identify key glycosyltransferase genes associated with patient prognosis. Angiogenesis assays were performed utilizing tumor-conditioned medium to assess the influence of GDP-fucose protein O-fucosyltransferase 2 (POFUT2) in cancer cells on human umbilical vein endothelial cells (HUVECs).Flag-Immunoprecipitation combining mass spectrometry detection was employed to identify potential interacting proteins with POFUT2.Western blot, immunoprecipitation, and immunohistochemistry were used to assess the interaction between POFUT2 and Junction Plakoglobin (JUP), as well as the correlation between the expression of Vascular endothelial growth factor A (VEGFA) and Platelet Endothelial Cell Adhesion Molecule-1 (CD31). Our analysis revealed that POFUT2 is significantly upregulated in CRC tissues and correlates with poor prognosis. Elevated POFUT2 expression in CRC cells enhances proliferation, invasion, and angiogenic capabilities of HUVECs. Among POFUT2 potential interacting proteins, three proteins were found to be involved in angiogenesis: JUP, HSBP1 (Heat Shock Factor Binding Protein 1), and AGO2 (Argonaute RISC Catalytic Component 2). Specifically, HSBP1 negatively regulates angiogenesis, whereas JUP and AGO2 positively regulate angiogenesis. Our results demonstrated that POFUT2 promotes the protein expression of JUP but does not affect the expression of AGO2. Further investigations revealed that POFUT2 interacts with JUP, upregulates its expression through fucosylation, and subsequently regulates VEGFA levels, thereby enhancing angiogenesis. A significant positive correlation was observed between POFUT2 and the expression levels of JUP, VEGFA, and CD31 in CRC tissues. POFUT2 is identified as a critical glycosyltransferase gene in CRC, closely associated with angiogenic phenotypes and poor prognosis. High POFUT2 expression in CRC regulates JUP fucosylation, increasing JUP and VEGFA levels, which promotes angiogenesis. These findings suggest POFUT2 could serve as a prognostic marker for colorectal cancer, and targeting it may inhibit angiogenesis and aid in treatment. - Source: PubMed
Publication date: 2026/01/01
Zou YanfengYang YianXu WeiCao PeiguoLi Zheng - Combination of radiotherapy (RT) and anti-PD-1 immunotherapy (IO) has shown significant efficacy in treating hepatocellular carcinoma (HCC). Nevertheless, yet the underlying mechanisms remain incompletely understood. A Hepa1-6 mouse HCC model was established to explore the anti-tumor mechanism of combination therapy in HCC. Notably, combination therapy effectively inhibited tumor growth in mice bearing Hepa1-6 tumors. Through MeRIP-sequencing, we indicated that combination therapy increased m6A modification and reduced mRNA expression of Hspb1, a negative regulator of ferroptosis, in tumors from mice. Both combination therapy and Hspb1 downregulation significantly induced Hepa1-6 cell ferroptosis. Metabolomics analysis revealed that Hspb1 downregulation further promoted abnormal lipid metabolism in Hepa1-6 tumor-bearing mice, enhancing pro-ferroptosis effects of combination therapy. Meanwhile, Hspb1 downregulation further enhanced RT and IO-induced anti-tumor immune response in tumor-bearing mice, as evidenced by significantly elevated numbers of cytotoxic CD8 + T cells. Additionally, combination therapy also significantly downregulated RNA demethylase Alkbh5 in tumor-bearing mice. Overexpression of Alkbh5 increased Hspb1 expression and inhibited ferroptosis, indicating that Alkbh5 regulates ferroptosis through targeting Hspb1. Targeting Alkbh5/Hspb1/ferroptosis axis may enhance anti-tumor effects in combination therapy, highlighting a potential therapeutic approach for HCC. - Source: PubMed
Publication date: 2025/12/19
Dou TingZhu XianggaoLi HongWang RunmeiHe JiepuGeng HongweiZhang WeiYu QinZhao HaipingYang Hao - Temperature changes during embryogenesis, through a process called embryonic thermal programming, can modify the long-term thermotolerance of broilers or the hepatic metabolism of mule ducks. This study focused on the very short-term impacts on mule duck livers of such a programming which consist of increasing the incubation temperature by + 1°C, 16h/24h, from the 13th to 27th day of embryonic development. Using fluidigm technology, we analysed the impact of this temperature change on the relative expression of 81 genes involved in various metabolic pathways closely or remotely related to the fattening of the liver of mule ducks. - Source: PubMed
Publication date: 2025/11/07
Andrieux CBiasutti SZwick L LMarchand MPanserat SHoussier M