Ask about this productRelated genes to: SERPINH1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: SERPINH1 Blocking Peptide
- Patients referred with an osteogenesis imperfecta (OI) phenotype exhibit marked genetic heterogeneity, and a substantial proportion may harbor variants associated with early-onset osteoporosis (EOO) or OI-mimicking disorders rather than classical collagenopathies. This study aimed to define the genetic spectrum and non-COL1A1/2 variant burden in a cohort clinically diagnosed with OI. - Source: PubMed
Publication date: 2026/04/30
Ozturk Fatma NihalKeskin Ece - Oligodendroglioma is a specific type of brain glioma, and relatively little research has been conducted on it. The expression and prognosis of serine protease peptidase inhibitor, branch H, member 1 (SERPINH1) in some malignant tumors have been studied, but the prognosis value and potential mechanism of this gene in oligodendroglioma have not been reported yet, and further research is needed. This study aims to reveal the expression characteristics and biological functions of SERPINH1 in oligodendroglioma cells, laying the foundation for targeted drug development. - Source: PubMed
Publication date: 2026/02/25
Chen XueLi ShunyaoZhao HuijuanDeng LanZhong Liyun - Ferroptosis, characterized by iron-dependent lipid peroxidation, has emerged as a pivotal cell death pathway in various diseases, yet its regulation during viral infection remains elusive. Here, we reveal that Newcastle disease virus (NDV) exploits the Golgi apparatus as a central hub to orchestrate ferroptotic cell death in tumor cells. NDV infection provokes robust Golgi stress and Golgiphagy, leading to the selective degradation of ARF1 (ARF GTPase 1), a GA-resident regulator of redox homeostasis, which in turn triggers a cascade of reactive oxygen species accumulation, lipid peroxidation, and ferroptosis. Mechanistically, we show that this process is dependent on the activation of the Golgi stress response and macroautophagy/autophagy-lysosome pathway. Importantly, inhibition of Golgi stress by exogenous spermine not only alleviates NDV-induced ferroptosis, but also demonstrates antiviral and cytoprotective effects, underscoring the translational potential of targeting the Golgi stress axis. Our findings uncover a previously unappreciated axis of virus-host interaction centering on Golgi stress and ferroptosis and suggest that modulation of organelle-specific stress responses represents a promising therapeutic strategy in both antiviral and cancer contexts.: AMPK: AMP-activated protein kinase; ARF1: ARF GTPase 1; ARF4: ARF GTPase 4; ATG7: autophagy related 7; BFA: brefeldin A; CGAS: cyclic GMP-AMP synthase; CHX: cycloheximide; CQ: chloroquine; CREB3: cAMP responsive element binding protein 3; DFO: deferoxamine; ER: endoplasmic reticulum; Fe: ferrous ions, GA: Golgi apparatus; GOLGA2/GM130: golgin A2; GPX4: glutathione peroxidase 4; GSH: glutathione; GSR: Golgi stress response; HCMV: human cytomegalovirus; HSV-1: herpes simplex virus 1; Lip-1: Liproxstatin-1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MDA: malondialdehyde; mtDNA: mitochondrial DNA; MTOR: mechanistic target of rapamycin kinase; NDV: Newcastle disease virus; NCOA4: nuclear receptor coactivator 4; PUFA: polyunsaturated fatty acid; ROS: reactive oxygen species; Rot: rotenone; SLC7A11: solute carrier family 7 member 11; SERPINH1/HSP47: serpin family H member 1; TFE3: transcription factor binding to IGHM enhancer 3; WT: wild-type. - Source: PubMed
Publication date: 2026/04/10
Kan XianjinYang MengqingXie GuangleiYin YuncongJiang HuiYuan YanmeiSun YingjieDing Chan - The extracellular matrix (ECM) plays a critical role in tumor progression by modulating cell adhesion, migration, and signaling; however, its contribution to metastatic progression in spontaneous mammary tumors remains poorly understood. Mammary tumors are among the most common neoplasms in female dogs and share histopathological and molecular similarities with human breast cancer, supporting their use as a comparative oncology model. To investigate ECM remodeling during tumor progression, we analyzed normal, non-metastatic, and metastatic canine mammary tissues using histological approaches and label-free quantitative proteomics. Publicly available human breast cancer transcriptomic datasets were interrogated for validation of conserved molecular signatures. Proteomic profiling identified 12 differentially expressed ECM-related proteins: eight were upregulated (COL12A1, COL4A1, COL4A2, SERPINH1, SERPINF1, HTRA1, TNC, PCOLCE) and four were downregulated (MMRN1, ABI3BP, DPT, OGN). The downregulated proteins were further validated in human breast cancer transcriptomes. Collectively, these findings indicate active ECM remodeling during tumor progression, characterized by increased expression of proteins associated with matrix stiffness and invasiveness. This study highlights evolutionarily conserved mechanisms of ECM dysregulation in breast cancer and identifies potential matrix targets for translational research and biomarker development. - Source: PubMed
Publication date: 2026/03/24
de Almeida Bruno SousaRocha Gisele VieiraNunes SimoneZanette Dalila LuciolaBatista MichelEstrela-Lima AlessandraRegis-Silva Carlos GustavoDamasceno Karine Araújo - Long non-coding RNAs (lncRNAs) play pivotal regulatory roles in mammalian male reproduction; however, the specific mechanisms governing testicular maturation and puberty onset in goats remain elusive. Here, we characterized the morphometric and transcriptomic profiles of Qianbei Ma goat testes at 0, 6, 12, and 18 months of age. We identified the 0 to 6-month interval as a critical window for testicular development, marked by rapid seminiferous tubule expansion and a surge in serum testosterone. This period coincided with extensive transcriptomic reprogramming, leading to the identification of a key regulator, lncRNA TCONS_00131158. Mechanistically, we constructed a competing endogenous RNA (ceRNA) network, demonstrating that TCONS_00131158 acts as a molecular sponge for miR-30c-3p, thereby derepressing its target gene, SERPINH1. Functional assays revealed that TCONS_00131158 knockdown impaired Leydig cell proliferation, induced apoptosis, and downregulated key steroidogenic enzymes (e.g., STAR, CYP11A1), reducing testosterone secretion. Conversely, SERPINH1 overexpression reversed miR-30c-3p-mediated repression, exhibiting pro-steroidogenic activity mirroring that of TCONS_00131158. This study elucidates the essential role of the TCONS_00131158/miR-30c-3p/SERPINH1 axis in regulating Leydig cell function and testosterone biosynthesis, offering a novel epigenetic marker for early selection of male reproductive potential in livestock. - Source: PubMed
Publication date: 2026/04/02
Tang WenCao MaoshengQiao FengxinLuo JinhongJu YonghongWang XiaodongAn PengchenChen Xiang