Ask about this productRelated genes to: SERPINH1 antibody
- Gene:
- SERPINH1 NIH gene
- Name:
- serpin family H member 1
- Previous symbol:
- CBP1, CBP2, SERPINH2
- Synonyms:
- HSP47, colligen
- Chromosome:
- 11q13.5
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-10
- Date modifiied:
- 2016-04-06
Related products to: SERPINH1 antibody
Related articles to: SERPINH1 antibody
- Ischemia-reperfusion injury (IRI) significantly impacts post-kidney transplantation (KTx), leading to delayed graft function (DGF) and potential graft loss. Current biomarkers and therapies for DGF and graft survival are inadequate. Immune cell infiltration after renal IRI is crucial in driving inflammation and injury. - Source: PubMed
Zhang YifeiLi YuqingQiu XuemengWu JiyueBi QingCao PengZhang JiandongWang Wei - The aggressive cancer known as Esophageal Squamous Cell Carcinoma (ESCC) has a dismal prognosis. Epigenetic changes such as demethylation have a significant impact on ESCC development and progression. - Source: PubMed
Publication date: 2026/06/08
Sheng YiMa JieLi YangYin ZihuanGao XukunLuo RuixingSheng BoxiangZhu XueyingZhang Renquan - During infection with highly pathogenic Avian Influenza virus (HPAIV), heat shock proteins (HSPs) play roles in host immune responses by interacting with various regulators of cell signaling pathways and in mediating cellular homeostasis. However, the tissue-specific regulation of these chaperones, particularly their potential association with the NF-κB pathway, remains poorly defined in avian species. Chickens were infected with HPAIV (A/chicken/Vietnam/NA01/2019 (H5N1), and the expression patterns of a comprehensive range of HSPs (small HSPs to canonical classes) were analyzed in lung and spleen at 1 and 3 days post-infection (dpi). As a result, HPAIV infection induced significant temporal up-regulation of mRNA of small sHSPs (sHSPs; HSPB7, HSPB9), HSPE1, and a collagen-specific molecular chaperone, SERPINH1, in both tissues. To investigate transcriptional regulation, DF-1 cells were stimulated with Poly(I: C) in the presence or absence of NF-κB inhibitors. Notably, NF-κB inhibition was associated with an up-regulation of HSPB9 and a depression of SERPINH1 in PIC-treated DF-1. These results suggest that specific HSPs may be influenced by pro-inflammatory signaling during viral infection, with NF-κB signalling potentially contributing to their negative regulation during viral stress response. Collectively, these findings provide preliminary insights into the complex molecular dynamics of HPAIV pathogenesis and highlight the importance of host-mediated signaling pathways in modulating the host cellular stress response in poultry. - Source: PubMed
Publication date: 2026/06/01
So Jae RungTruong Anh DucNguyen Thu UyenBugenyi Andrew WangeTran Ha Thi ThanhDang Hoang VuSong Ki-Duk - CADASIL is a hereditary cerebral small vessel disease caused by NOTCH3 mutations, leading to age-dependent vascular and neurological impairments. Despite its clinical impact, the underlying pathogenic mechanisms remain poorly understood, partly because existing murine models often fail to fully replicate the broad pathological spectrum observed in humans. Here, we established and characterized a novel zebrafish (Danio rerio) model carrying the Notch3 p.C680S mutation. Our mutant zebrafish mimicked key age-related CADASIL features, including cerebrovascular dysfunction, telencephalic atrophy, cognitive impairment, and the deposition of granular osmiophilic material (GOM). Integrated transcriptomic and proteomic analyses revealed a significant downregulation of type IV collagen-related molecules, including serpinh1b, col4a1, and col4a2. These molecular findings were corroborated by immunostaining, which confirmed reduced perivascular accumulation of type IV collagen around cerebral blood vessels. Furthermore, AlphaFold 3-based structural modeling categorized the p.C680S variant as a "nonconventional" NOTCH3 mutation. These findings validate the zebrafish as a valuable vertebrate model for CADASIL and raise the possibility that diminished type IV collagen levels contribute to CADASIL pathogenesis, particularly in cases of nonconventional NOTCH3 mutations. - Source: PubMed
Publication date: 2026/06/03
Kanoh TohgoOubayashi ShihoFurukawa KengoFujimoto KosukeInoue AmaneMizoguchi TakamasaYamaguchi MasashiTakahashi-Nakaguchi AzusaHasegawa YoshinoriOhara OsamuAoki IchioItoh Motoyuki - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by immune cell dysfunction. The endomembrane system, consisting of the endoplasmic reticulum (ER) and Golgi apparatus (GA), plays a central role in protein synthesis and trafficking. However, the regulatory architecture of the ER-Golgi axis in RA immune cells remains incompletely understood. - Source: PubMed
Publication date: 2026/05/15
Shi YangnaZhang WeiLi ChenxiLiu FannaYin LianghongLiu DongzhouHong XiaopingZeng ZhipengLi HaitaoDai YongTang DongeGong Wenyu