Ask about this productRelated genes to: SENP5 antibody
- Gene:
- SENP5 NIH gene
- Name:
- SUMO specific peptidase 5
- Previous symbol:
- -
- Synonyms:
- MGC27076
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-20
- Date modifiied:
- 2018-02-23
Related products to: SENP5 antibody
Related articles to: SENP5 antibody
- Limbic white matter (WM) abnormalities are prevalent in aging and Alzheimer's disease (AD), but genetic drivers are unclear. - Source: PubMed
Lorenz Anna SSathe AditiYang YisuDurant AlainaWu YiyangKim Michael EGao ChenyuNewlin Nancy RRamadass KarthikKanakaraj PraitayiniKhairi Nazirah MohdLi ZhiyuanYao TianyuanHuo YuankaiDumitrescu LoganShashikumar NiranjanaPechman Kimberly RRisacher Shannon LBeason-Held Lori LAn YangArfanakis KonstantinosErus GurayDavatzikos ChristosHabes MohamadWang DiTosun DuyguToga Arthur WThompson Paul MMormino Elizabeth CZhang PanpanSchilling KurtAlbert MarilynKukull WalterBiber Sarah ALandman Bennett AJohnson Sterling CBendlin BarbaraSchneider JulieBennett David AJefferson Angela LResnick Susan MSaykin Andrew JBelow Jennifer EHohman Timothy JArcher Derek B - Cancer is a complex set of diseases caused by the dysregulation of cell proliferation, differentiation, and apoptosis, ultimately leading to malignant tumor development and metastasis. Recent studies have revealed that dysregulation of N4-acetylcytidine (acC) acetylation is associated with enhanced metastatic potential and tumor progression in various cancer types. However, it remains unclear whether diverse cancer types share common epitranscriptomic regulatory patterns or engage in interconnected networks. - Source: PubMed
Publication date: 2026/05/19
Yin XiangyuTu GangWang XuanLiu YuqiWang YueMa JiongmingYu XiaoXuanMeng JiaSong Bowen - 3q29 deletion (3q29Del) syndrome is caused by a 1.6 Mb copy number variant (CNV) located near the telomeric end of the long arm of the third human chromosome. Hemizygosity of this set of 22 protein-coding genes significantly increases risk for schizophrenia and autism spectrum disorders among other neurodevelopmental conditions, but it is not known which genes in this CNV interval are responsible for these phenotypes. We have evaluated existing literature and public genomic resources for this set of genes, categorizing them based on known cellular functions and assessed their potential as phenotypic drivers. We provide a comprehensive, synthetic review of the essential known functions of 3q29 deleted genes, and how multiple 3q29-encoded proteins may functionally interact. Our analysis reveals that ubiquitination/SUMOylation stands out among processes potentially compromised due to compound haploinsufficiency of four 3q29Del genes (UBXN7, FBXO45, RNF168, SENP5). The available genomic evidence indicates that no single gene in the 3q29 locus is solely responsible for the neurodevelopmental phenotypes of 3q29Del syndrome. Overall, we propose that functional, expression, and gene constraint evidence supports six genes (TFRC, UBXN7, FBXO45, PAK2, NCBP2, DLG1) as the most likely phenotypic drivers in 3q29Del syndrome. Haploinsufficiency of these proteins would likely disrupt metabolic, synaptic, and signaling mechanisms in developing and mature neurons, which collectively may impair neural circuit differentiation and function. - Source: PubMed
Publication date: 2026/04/21
Herriges Allyson RPurcell Ryan H - BACKGROUND: Post-translational modifications (PTMs) play a critical role in regulating innate immune responses, including type I interferon (IFN) production and JAK-STAT pathway activation. However, the role of deSUMOylation in antiviral defense remains unclear. RESULTS: We identify Sentrin/SUMO-specific protease 5 (SENP5) as a positive regulator of the phosphorylation of STAT2 in JAK-STAT pathway via its deSUMOylation activity, thus inhibiting VSV or HSV-1 replication, and strengthening the antiviral activity of IFN-α. Further investigation reveals that SENP5-mediated deSUMOylation of Aurora kinase A (AURKA) alleviates its inhibition of STAT2 phosphorylation and antiviral innate immunity. Finally, AURKA suppresses STAT2 phosphorylation, and negatively regulates antiviral innate immunity by enhancing the activity of protein phosphatase 2 A (PP2A). CONCLUSIONS: Our study demonstrates that SENP5 upregulates STAT2 phosphorylation via the AURKA–PP2A–STAT2 axis, and uncovers a previously uncharacterized role of SENP5 in regulating antiviral innate immunity. - Source: PubMed
Publication date: 2026/03/13
Song ShuyiKan YuweiZhou MinghuiJiang YanjunTang YitianLuo HongchunHu Yuan - SUMOylation is a critical post-translational modification of proteins. However, the roles of SUMOylation-related genes in regulating the tumor immune microenvironment and their potential as therapeutic targets in CRC remain unclear. We integrated transcriptomic data from TCGA and GEO to identify 200 SUMOylation-related genes associated with prognosis. Among these, 58 genes exhibiting significant survival differences were selected and classified into three distinct clusters. Cluster C patients have the worst prognosis, linked to increased tumor proliferation and weakened immune responses. The LASSO combined with Random Survival Forest (RSF) approach demonstrated optimal performance in ten machine learning algorithms, yielding the highest C-index (0.715). Subsequently, six key genes—SENP7, NUP85, UHRF2, BRCA1, TOPORS, and SENP5—were selected using the LASSO-RSF framework to develop a refined prognostic model. This model demonstrated high predictive accuracy, with 1-, 3-, and 5-year overall survival AUC values of 0.943, 0.961, and 0.981, respectively. Furthermore, the risk score derived from the model was significantly correlated not only with tumor metastasis and recurrence, advanced tumor stage, and patient age, but also with immune cell infiltration, tumor mutational burden, and sensitivity to anticancer drugs. Single-cell analysis revealed that the core gene UHRF2 is highly expressed in CD8 + exhausted T cells, but exhibits low expression in conventional CD8 + T cells and natural killer cells. Experimental data demonstrated that UHRF2 was upregulated in CRC and linked to poor prognosis. Silencing UHRF2 markedly inhibited both proliferation and migration of tumor cells in vitro, as well as tumor growth in vivo. In conclusion, the prognostic model derived from SUMOylation-related genes demonstrates robust predictive accuracy for patient outcomes. UHRF2 is associated with immunosuppression and promotes CRC progression, positioning it as a promising therapeutic target in CRC. - Source: PubMed
Publication date: 2026/02/27
Huang MeiQin YanYang QiongChen XueqingChen Kequan