SUMO3 polyclonal antibody
- Known as:
- SUMO3 pab (anti-)
- Catalog number:
- PAB10320
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SUMO3 polyclonal antibody
Related genes to: SUMO3 polyclonal antibody
- Gene:
- SUMO3 NIH gene
- Name:
- small ubiquitin like modifier 3
- Previous symbol:
- SMT3H1
- Synonyms:
- SMT3A
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-29
- Date modifiied:
- 2019-02-18
Related products to: SUMO3 polyclonal antibody
Related articles to: SUMO3 polyclonal antibody
- Non-small cell lung cancer (NSCLC) remains a major cause of cancer mortality worldwide, and radioresistance significantly compromises the efficacy of radiotherapy. However, the precise molecular determinants governing NSCLC radiosensitivity remain incompletely defined. Here, we identify SEPT5 as a key regulator of radioresistance, which is aberrantly upregulated in radioresistant NSCLC tissues and cell lines. Mechanistically, reduced expression of the deSUMOylase SENP3 leads to enhanced SUMO3 conjugation of SEPT5 at Lysine 296, thereby protecting it from ubiquitin-proteasome degradation. Accumulated SEPT5 then exerts a dual regulatory effect on the E3 ubiquitin ligase UBE3B. SEPT5 facilitates PCBP3 binding to the 3'-UTR of UBE3B mRNA, stabilizing the transcript and upregulating UBE3B expression. Concurrently, SEPT5 directly recruits UBE3B to promote K48-linked ubiquitination of GSDME at lysines 39 and 120, triggering its proteasomal degradation and suppressing irradiation-induced pyroptosis. Functionally, SEPT5 depletion restores GSDME-dependent pyroptosis and sensitizes NSCLC cells to radiotherapy in vitro and in vivo. More significantly, targeting SEPT5 potentiates the cytotoxic function of tumor-infiltrating CD8 T cells and cooperatively represses NSCLC progression when combined with anti-PD-1. Collectively, these findings define an integrated mechanism in which SUMOylation-dependent stabilization of SEPT5 and UBE3B-mediated GSDME degradation converge to suppress pyroptosis and attenuate antitumor immunity, positioning the SEPT5 regulatory axis as a potential therapeutic vulnerability to overcome radioresistance and enhance the efficacy of immunotherapy. - Source: PubMed
Publication date: 2026/09/15
Wen JunmiaoZheng WangWang BoyanLi HuitingJabbour SalmaShao ChunlinFan MinChen Jiayan - Leaf senescence, the final stage of leaf development, is regulated by complex interplays of intrinsic genetic programs and environmental cues. Throughout their lifetimes, all living organisms encounter various endogenous and environmental challenges, many of which can cause potentially fatal DNA damage. Among these, DNA-protein crosslinks (DPCs) are particularly deleterious, as they obstruct essential processes such as replication and transcription, thereby compromising genome integrity and ultimately leading to premature aging across species. However, the biological significance of DPCs and their repair mechanisms in leaf senescence remains unexplored. Here, we demonstrate that cis-platin (cis-Pt), a potent DPC inducer, accelerates leaf senescence in Arabidopsis. We reveal that Arabidopsis DPC repair factor WSS1A, a WLM/Spr-T metalloprotease, plays a negative role in leaf senescence induced by cis-Pt treatment, darkness, and leaf age. WSS1A forms nuclear condensates via liquid-liquid phase separation both in vitro and in vivo, which is cooperatively driven by its N-terminal segment and intrinsically disordered region. Mechanistically, WSS1A non-covalently interacts with SMALL UBIQUITIN MODIFIER 3 (SUMO3) through its SUMO-interacting motif and is also covalently SUMOylated by SUMO3. Genetic analysis further reveals that WSS1A and SUMO3 act in the same pathway to control cis-Pt-induced leaf senescence. Together, this study establishes a conceptual framework connecting DPC repair and SUMO3-dependent regulation of WSS1A in modulating leaf senescence in Arabidopsis. - Source: PubMed
Park SanghoonOh HyunwooJeong UkcheolLee Jae HoChoi HyeyoungPark HyunsuKim JinkwangKim YongminKwak JunminYoon Yeong SeonLi ZhonghaiLee Jong-ChanWoo Hye Ryun - Small ubiquitin-like modifiers (SUMOs) are small peptides conjugated to proteins during post-translational modification, which have been reported to modulate several aspects of the immune system, notably in autoimmune disorders. - Source: PubMed
Publication date: 2026/07/20
Giblin Sean PMoiseanu Vlad RazvanCarrington Christina JosephineNaing AudreyWatkins KillianTsuchiya TomokoKanegasaki ShiroPease James Edward - This study investigated the cytokine profiles and expression patterns of chromosome 21 genes in Saudi Arabian children with Down syndrome (DS) to identify molecular drivers of immune dysregulation and pulmonary complications. This case-control study enrolled 116 children with DS and 60 healthy controls. Cytokine levels Interleukin (), , Vascular Endothelial Growth Factor (), Tumor Necrosis Factor-alpha (), Monocyte Chemoattractant Protein-1 (), , Interferon-gamma (), and Transforming Growth Factor-beta () were measured at baseline and after lipopolysaccharide (LPS) stimulation using the Meso Scale Discovery (MSD) V-PLEX platform. Gene expression analysis was performed on a panel of immune-related (Small Ubiquitin-Like Modifier 3 (), Runt-Related Transcription Factor 1 (), Autoimmune Regulator (), and Regulator of Calcineurin 1 ()) and pulmonary genes (DNA Methyltransferase 3 Like (), Dual Specificity Tyrosine Phosphorylation Regulated Kinase 1 A (), , , , and Integrin Subunit Beta 2 (CD18) located on chromosome 21 using quantitative real-time PCR (qRT-PCR). Children with DS exhibited elevated levels of pro-inflammatory cytokines (, , , ) and the anti-inflammatory cytokine compared to controls, both at baseline and after LPS stimulation ( < 0.05). Gene expression analysis revealed upregulation of immune-related genes (, , , ) and pulmonary genes (, , , , , ) in the DS group. and emerged as strong predictors of DS, while , , and revealed potential as biomarkers for pulmonary complications. receiver operating characteristic (ROC) analysis identified (AUC: 0.935) and (AUC: 0.890) as strong predictors of the DS immune phenotype. Furthermore, (AUC: 0.966), (AUC: 0.913), and (AUC: 0.944) demonstrated superior diagnostic accuracy as potential biomarkers for DS-associated pulmonary abnormalities. This study provides a comprehensive insight into the immune dysregulation and genetic predisposition in Saudi Arabian children with DS. The findings highlight potential biomarkers (, , , , , , , , ) and therapeutic targets for personalized medicine approaches to manage immune dysfunction and respiratory complications in this population. - Source: PubMed
Publication date: 2026/06/02
Elmetwalli AlaaEl-Sakka Samaa AhmedAlzahrani Othman RAl Balawi Aisha NawafSalama Afrah FatthiHassan Mervat GElsayed AshrafWael DaliaAlaa E Sorour HebaEl-Sewedy Tarek - SUMOylation has emerged as a key regulator of chromatin and transcription, yet its contribution to lineage reprogramming remains unclear. To explore how chromatin SUMOylation influences cellular plasticity, we studied CEBPA-driven lineage reprogramming of human leukemic B-cells into macrophage-like cells. By integrating ChIP-seq, ATAC-seq, RNA-seq and chromatin-directed proteomics, we mapped the chromatin landscape and transcriptomic changes during early reprogramming. Lineage conversion triggered a dynamic rise in SUMO2/3 chromatin occupancy at CEBPA-bound sites, revealing a coordinated regulatory mechanism. Proteomic profiling of SUMO2/3- and CEBPA-associated chromatin uncovered extensive convergence and enrichment of differentiation-related transcription factors, chromatin remodelers and coregulators. Among these, NCOA3 displayed markedly increased SUMO2/3 association upon lineage conversion. NCOA3 co-occupied CEBPA- and SUMO2/3-bound chromatin regions, implying a SUMOylation-supported coregulatory role in lineage reprogramming. Pharmacological inhibition of SUMOylation using ML-792 (SUMOi) selectively enhanced CEBPA chromatin occupancy and chromatin accessibility, altered the CEBPA association of proteins, and modified NCOA3 binding dynamics. SUMOi also reshaped gene expression, promoting loss of B-cell identity and activation of macrophage-associated programs, including lipid metabolism. Collectively, our findings highlight chromatin SUMOylation as a dynamic and context-dependent modifier that fine-tunes lineage transitions, with implications for chromatin biology and therapeutic modulation of cell identity. - Source: PubMed
Publication date: 2026/05/27
Valima EmmaManjur A B M KaiserSavinainen EeviVaris VeraLaunonen Kaisa-MariGraf ThomasVarjosalo MarkkuNiskanen Einari APalvimo Jorma J