Ask about this productRelated genes to: NOSIP antibody
- Gene:
- NOSIP NIH gene
- Name:
- nitric oxide synthase interacting protein
- Previous symbol:
- -
- Synonyms:
- CGI-25
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-06
- Date modifiied:
- 2016-10-24
Related products to: NOSIP antibody
Related articles to: NOSIP antibody
- [This corrects the article DOI: 10.3389/fimmu.2026.1755657.]. - Source: PubMed
Publication date: 2026/07/21
Li ShihuiTamai ToshikatsuShinzawa YuiFujisawa SotaroTanabe YamatoUtsunomiya MakotoNakagawa HidetoshiKurachi JunkoKoura MikiMizukoshi EishiroKurachi Makoto - Type I collagen is the most abundant form of collagen and forms the organic component of bone. Pathogenic variants in genes encoding its constituent polypeptide chains, and , can result in autosomal dominant osteogenesis imperfecta and other connective tissue disorders. Although osteogenesis imperfecta is clinically well-described, the molecular basis of clinical heterogeneity among patients is not well understood. We undertook a global proteomic approach to uncover alterations in osteogenesis imperfecta patient bone-derived stromal cells as well as their secretome. We performed multiplexed tandem mass tag (TMT)-based proteomics analysis of cells from three patients along with three controls to investigate global changes in the proteome of these cells as well as their secretome. This was combined with analysis of proline hydroxylation to catalog the modification of type I collagens in this disorder. We observed significant changes in both the cellular and secreted proteomes including the levels of proteins involved in osteoblast proliferation such as nitric oxide synthase-interacting protein (NOSIP), secreted frizzled-related protein 1 (SRFP1) and transforming growth factor beta-1-induced transcript 1 protein (TGFB1I1) as well as others involved in endoplasmic reticulum homeostasis such as protein disulfide isomerase A6 (PDIA6) and reticulophagy regulator 3 (RETREG3). Notably, a number of alterations were observed in proline hydroxylation in intracellular collagens - COL1A1 and COL1A2. These findings expand our current understanding of the cellular pathophysiology in osteogenesis imperfecta and could lead to the identification of novel therapeutic targets. - Source: PubMed
Publication date: 2026/07/22
Garapati KishoreMun Dong-GiDevasahayam Arokia Balaya RexSaraswat MayankRenuse SantoshTrahan GregoryKandasamy Richard KDeyle David RPandey Akhilesh - Chronic antigen exposure drives CD8 T cell exhaustion; however, strategies to maintain a long-lived, functional CD8 T cell population under chronic stimulation remain unclear. In this study, we demonstrate that overexpression of nitric oxide synthase-interacting protein (NOSIP) enhances the persistence of antigen-specific CD8 T cells under chronic antigen stimulation. Notably, NOSIP overexpression preserved a less differentiated CX3CR1 subset and inhibited its progression toward an apoptosis-prone CX3CR1 state, which was associated with reducing cell death and promoting long-term persistence. In a tumor model, NOSIP-overexpressing CD8 T cells exhibited improved tumor control, indicating that NOSIP-mediated persistence confers superior antitumor capacity. Furthermore, NOSIP overexpression increased the responsiveness of CD8 T cells to programmed death-ligand 1 blockade, suggesting that NOSIP may represent a promising therapeutic target. - Source: PubMed
Publication date: 2026/06/22
Li ShihuiTamai ToshikatsuShinzawa YuiFujisawa SotaroTanabe YamatoUtsunomiya MakotoNakagawa HidetoshiKurachi JunkoKoura MikiMizukoshi EishiroKurachi Makoto - Kidney cancer is one of the most common malignancies of the urinary system, with early surgical resection and molecular targeted therapy being the primary treatment options for clear cell renal cell carcinoma (ccRCC). Nitric oxide synthase interacting protein (NOSIP) has been implicated in several types of malignancies; however, its role in ccRCC remains elusive. In this study, we employed a variety of techniques, including transfection, co-immunoprecipitation (co-IP), real-time polymerase chain reaction (RT-PCR), Western blotting, ubiquitin assay, and animal experiments, to explore the role of NOSIP in renal cancer cells. Our results demonstrated that NOSIP interacts with SPTAN1 and promotes the progression of ccRCC by facilitating the ubiquitination and degradation of SPTAN1, thus downregulating its expression. Elevated SPTAN1 levels were found to inhibit the proliferation and metastasis of ccRCC, while the downregulation of SPTAN1 reversed the inhibition of cell survival caused by NOSIP knockdown. Moreover, xenograft studies in nude mice confirmed that NOSIP promotes tumor growth in vivo. This work identifies NOSIP as a key player in the proliferation and apoptosis of ccRCC and suggests that it contributes to malignancy of ccRCC by modulating SPTAN1 expression in an ubiquitination-dependent manner. Our findings provide a theoretical basis and experimental foundation for early diagnosis and molecular targeted therapy of ccRCC. - Source: PubMed
Publication date: 2026/06/23
Cao RuoxueLian BiPan XueshanGao JunjieYang DandanSun KangLian ChaoqunMa JiaWang ZhiweiXia JunCao Tong - Renal cell carcinoma (RCC) is a malignant tumor of the urinary system with a high incidence. Due to limited treatment options and poor prognosis, novel therapeutic strategies are urgently needed. Recent studies revealed that Nosip participates in cell growth regulation by activating endothelial nitric oxide synthase (eNOS) and mediating the ubiquitination of erythropoietin receptor, suggesting its potential role as an oncogene in RCC progression. - Source: PubMed
Publication date: 2026/03/27
Wang JiaoHuang ZhengYang DandanGao JunjieXu QingDai MengluXia JunMa JiaPan Xueshan