Ask about this productRelated genes to: SPINK6 antibody
- Gene:
- SPINK6 NIH gene
- Name:
- serine peptidase inhibitor, Kazal type 6
- Previous symbol:
- -
- Synonyms:
- MGC21394, UNQ844, BUSI2
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-30
- Date modifiied:
- 2015-08-26
Related products to: SPINK6 antibody
Related articles to: SPINK6 antibody
- The SPINK2 protein, encoded by the SPINK2 gene, plays an essential role in the normal development of spermatozoa, and its deficiency is associated with spermatogenesis disorders ranging from aspermia to azoospermia. This study aimed to identify the most deleterious variants of the SPINK2 gene and to evaluate their effects on protein structure and function through an in silico approach. A total of 8,028 variants were identified, including 72 missense variants. Using 11 bioinformatics tools, six variants (P50L, T58I, C66Y, E62A, P42S, and P45L) were predicted to have deleterious effects. Protein-protein interaction analysis using the STRING database revealed strong functional associations between SPINK2, SPINK1, and ACR, and medium-confidence associations with SPINK4, SPINK13, PMPCA, KLK4, SPINK9, SPINK6, SPACA1, and NUDT8. Local structural analysis showed that variants such as T58I and C66Y gained additional hydrophobic interactions, whereas P50L and P42S lost key interactions, potentially impairing protein stability and function. Molecular dynamics simulations using GROMACS revealed that P50L enhances protein stability, reduces amino acid flexibility, and increases the overall dimensions of the protein. T58I had a mild effect on stability, whereas E62A and C66Y decreased stability and flexibility while increasing protein size. P42S and P45L induced slight stability alterations, reduced flexibility, and enlarged the protein. Overall, these structural and dynamic changes suggest functional impairment of SPINK2. To our knowledge, this is the first study to identify six deleterious SPINK2 variants with potential roles in the disruption of spermatogenesis, providing a foundation for future functional and clinical investigations. - Source: PubMed
Publication date: 2026/01/30
Elkarhat GhitaAit Benichou SamahRedouane SalaheddineBarakat AbdelhamidSoukri AbdelazizEl Khalfi BouchraRouba Hassan - Head and neck squamous cell carcinoma (HNSCC) is a heterogeneous malignancy with poor prognosis. Dysregulation of E2F transcription factors (E2Fs), which control cell proliferation and apoptosis, is implicated in HNSCC pathogenesis. This study explores HNSCC molecular heterogeneity via E2Fs expression, identifies distinct subtypes, and develops a prognostic model that integrates gene expression, immune infiltration, and drug sensitivity. - Source: PubMed
Publication date: 2025/04/24
Jiang HuanyuZhou LijuanZhang HaidongYu Zhenkun - Tumor metastasis is the main cause of hepatocellular carcinoma (HCC) related death. Loss of cell polarity may lead to weakened cell adhesion, epithelial-mesenchymal transition (EMT), and metastasis of HCC. However, the mechanism involved in HCC cells polarity loss is still less studied. Here, we found that BAP31 expression increased with tumor grade and metastasis. Moreover, BAP31 silencing inhibited invasion and migration and recovered the polarity of HCC cells. RNA-seq identified SPINK6 was a downstream gene of BAP31, and was associated with tumor stage and metastasis in HCC. IP-MS and IF assays showed that BAP31 bound to the RNA binding protein ELAVL1, and promoted its maturation. In addition, RIP, RNA-FISH, RNA stability and luciferase reporter assays confirmed that ELAVL1 could bind to the 3 'UTR region of SPINK6 mRNA to stabilize its expression. Depletion of SPINK6 inhibited the invasion and migration, re-established the cell polarity and suppressed EMT in HCC cells, while overexpression of SPINK6 partially counteracted BAP31/ELAVL1 knockdown caused attenuation of metastasis and recovery of polarity. Finally, experiments verified that BAP31-ELAVL1-SPINK6 axis induced cell polarity loss and promoted metastasis in HCC. Our study shed new light on the mechanism of cell polarity loss and metastasis in HCC. - Source: PubMed
Publication date: 2025/02/03
Zhang XiyangWang JingLiang XiaohuaJiang DongboSun YuanjieHu ChenchenHu FeimingHe YuanliSun YuboZhang JunqiDing JiaqiCai SiruiWang YueyueYang ShuyaYang Kun - Lentiviral vectors (LVs) are crucial tools in gene therapy and bioproduction, but high-yield LV production systems are urgently needed. Using clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR-associated protein 9 high-throughput screening, we identified nine critical genes (, and ) from 17,501 genes that limit LV packaging and formation. Knocking out these genes in HEK293T cells significantly increased virus production, with knockout exhibiting a 6.63-fold increase. Studies on multigene knockouts demonstrated that the cumulative effects of different gene knockouts can significantly enhance lentivirus production in HEK293T cells. Triple knockout of , and increased LV titer by ∼8.33-fold, and knockout (or knockdown) of and increased LV titer by ∼6.53-fold. This study established HEK293T cell lines with multiple genes knockout for efficient LV production, providing reliable technical support for LV production and application and offering new perspectives for studying LV packaging mechanisms and related virus research. - Source: PubMed
Publication date: 2024/10/16
Xinyue ZhangLi SiweiYujie WangYingcai DaiChanghao BiXueli Zhang - - Source: PubMed
Publication date: 2024/10/09
Ge JieyuYou MengxiangFan YuZhou YongJin LiZhai GuangtaoLiu FanWang Sijia