SSRP1 antibody - middle region (P100799_P050)
- Known as:
- SSRP1 (anti-) - middle region (P100799_P050)
- Catalog number:
- p100799_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SSRP1 antibody - middle region (P100799_P050)
Related genes to: SSRP1 antibody - middle region (P100799_P050)
- Gene:
- SSRP1 NIH gene
- Name:
- structure specific recognition protein 1
- Previous symbol:
- -
- Synonyms:
- FACT80
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-21
- Date modifiied:
- 2016-10-05
Related products to: SSRP1 antibody - middle region (P100799_P050)
Related articles to: SSRP1 antibody - middle region (P100799_P050)
- We have determined that the FACT (Facilitates Chromatin Transcription) complex components, SPT16 and SSRP1, associate with both the RPA (Replication Protein A) complex and adenovirus DNA-binding protein (DBP) within viral replication compartments (VRCs) during both human adenovirus 5 (Ad5) and adenovirus 12 (Ad12) infection, and possess proviral activities. Inactivation of FACT by the curaxin, CBL0137, reduces Ad5 and Ad12 E1A-dependent induction of early gene products, while inhibition of FACT by siRNA similarly affected Ad5 gene product synthesis, but differentially affected Ad12 gene product expression. A consistent feature of FACT inhibition, however, was a significant reduction in the protein levels of DBP, which correlated positively with a significant reduction in the formation of VRCs during infection, and the production of new, infectious virus. Pertinently, the inactivation of FACT with CBL0137 or siRNA increased the levels of the p53 protein and p53 target gene product, p21; FACT inhibition by CBL0137 limited the ability of E1A to induce S-phase in Ad-infected cells. We propose, therefore, that the FACT complex cooperates with E1A to promote early gene expression and create an environment conducive to viral replication, while FACT inactivation, through its ability to modulate VRC formation and cell cycle progression, has antiviral properties.IMPORTANCEViruses have evolved to inhibit cellular proteins and pathways that possess inherent antiviral activity and utilize cellular proteins and pathways that possess proviral activities. Identification and characterization of both antiviral and proviral factors are therefore important toward understanding the biology of virus-host interactions and the generation of novel antivirals. Viral replication compartments (VRCs) are essential for a productive infection; they are highly dynamic, spatially organized structures to which both proviral and antiviral cellular factors are recruited. Adenoviruses recruit cellular proteins, such as the RPA complex, to VRCs, though their precise roles during infection are poorly understood. Identification and characterization of cellular, RPA complex-associated proteins at VRCs are important to understanding their multifaceted roles during infection. The studies described herein further our understanding of the relationship between adenovirus, the RPA complex, and VRCs during infection, establish proviral roles for the FACT complex, and identify FACT inhibitors as potential antivirals for adenovirus infection. - Source: PubMed
Publication date: 2026/05/26
Sharmin TaranaZhao MoxuanManivannan SelvambigaiAlharbi KholoudSingh KaveriQashqari Fadi S IDavis SimonWard Douglas GTurnell Andrew S - Hepatocellular carcinoma (HCC) is a top cause of cancer-related death globally, with late diagnosis due to nonspecific early symptoms. Current single-factor prognostic models cannot reflect tumor heterogeneity, so a comprehensive tool for risk stratification and personalized treatment is needed. - Source: PubMed
Publication date: 2026/04/19
Li ZehaoZhong BoqiangZhang QianSun LinLi XiaoxiaoHu Xiao - The FAcilitates Chromatin Transcription (FACT) complex, comprising structure-specific recognition protein 1 (SSRP1) and suppressor of Ty 16 (SPT16), plays a key role in regulating gene transcription by facilitating ATP-independent nucleosome assembly. SSRP1 contains an HMG domain that binds to DNA and regulates cell proliferation, apoptosis, and DNA repair. However, its role in plant development remains poorly understood. In this study, we identified a mutant, small kernel 301 (smk301), characterized by reduced kernel size and semi-dwarfism. Map-based cloning revealed that the mutation affects ZmSSRP1 on chromosome 8, which is expressed throughout maize (Zea mays L.) tissues. ZmSSRP1 localizes to the nucleus and interacts with ZmSPT16 to form the FACT complex. Using RNA-seq and ATAC-seq analyses, we identified 3 candidate target genes involved in hormone pathways, all of which show a significant positive correlation with ZmSSRP1 expression. Notably, ZmSSRP1 was enriched in the chromatin open region of brassinosteroid-deficient dwarf 1 (ZmBRD1), which encodes a Brassinosteroid C-6 Oxidase. This indicates that ZmSSRP1 affects maize development by regulating the transcription of ZmBRD1, thereby influencing the brassinosteroid content in maize. Our findings shed light on how the FACT complex influences maize development by modulating the expression of brassinosteroid-related genes, offering insights into the molecular mechanisms underlying plant growth. - Source: PubMed
Wu JiawenWang YuZheng GuangmingYan RuyuPu MenglinZhao YajieZhang ZhimingDing HaipingWang YanyanLuo ChaoZhang XianshengZhou ChaoZhao Xiangyu - AACOCF3, a cell-permeable arachidonic acid analogue, is widely established as a selective inhibitor of cytosolic phospholipase A2 (cPLA2, PLA2G4A) in studies of metabolic disorders. Although its primary mechanism involves cPLA2 inhibition, emerging evidence indicates that AACOCF3 may target additional protein entities, exemplified by calcium-independent phospholipase A2 (iPLA2, PLA2G6) and fatty acid amide hydrolase (FAAH). Notably, cPLA2 displays a markedly heterogeneous expression profile in non-small cell lung cancer (NSCLC). Our findings establish that AACOCF3 exerts more potent growth inhibition in cPLA2-negative NSCLC cells, with IC50 values of 15.13 μM for H1975 and 15.84 μM for PC9 cells, in contrast to the cPLA2-positive A549 cells (IC50 = 56.23 μM). Mechanistically, AACOCF3 upregulates IFN-α/β signaling-associated genes (e.g., IFNB1, ISG15) specifically in cPLA2-negative NSCLC cells. This aligns with TCGA-LUAD data revealing that PLA2G4A-low tumors predominantly engage immune-activation pathways rather than metabolic programs when compared to PLA2G4A-high counterparts. Through integrated molecular docking and surface plasmon resonance (SPR) analysis, we identified structure-specific recognition protein 1 (SSRP1) as a direct molecular target of AACOCF3 in cPLA2-negative NSCLC, with SPR binding studies confirming a stable interaction (Kd = 25.9 μM). Ectopic SSRP1 expression abrogated AACOCF3-induced phenotypic alterations, concurrently suppressing IFN-α/β signaling. Collectively, these results provide evidence that AACOCF3 exerts its anti-proliferative effect by targeting SSRP1, which leads to the activation of the IFNα/β pathway, thereby underscoring its therapeutic promise for the cPLA2-negative patient subpopulation. - Source: PubMed
Publication date: 2026/01/14
Wang HongboWen ZihaoJia YupengTong XinyuWang WeifangWang ZeJin HongkaiGao XiaoyaTao XinyuanCheng HaoLi TingtingLi ShinanChen TingtingLi KunfangLi Bo - Aberrant epigenetic regulation is a hallmark of diffuse midline glioma (DMG), an incurable pediatric brain tumor. The H3K27M driver histone mutation leads to transcriptional dysregulation, indicating that targeting the epigenome and transcription may be key therapeutic strategies against this highly aggressive cancer. One such target is the facilitates chromatin transcription (FACT) histone chaperone. We found FACT to be enriched at developmental gene promoters, coinciding with open chromatin and binding motifs of core DMG regulatory transcription factors. Furthermore, FACT co-occurred with the bromodomain and extraterminal domain (BET) protein BRD4 at promoters and enhancers, suggesting functional cooperation between FACT and BRD4 in DMG. In vitro, a combinatorial therapeutic approach using the FACT inhibitor CBL0137, coupled with BET inhibition, revealed potent and synergistic cytotoxicity across a range of DMG cultures. These results were recapitulated in vivo, extending survival in three independent orthotopic patient-derived xenograft models of DMG. Mechanistically, we show that CBL0137 treatment decreased chromatin accessibility and combined with BET inhibition to cause broad transcriptional collapse; silencing of several key oncogenes including , , , and ; and alterations to the splicing landscape. This combination also elicited immune-related effects, including activation of the interferon response and antigen presentation mechanisms in DMG cells and induction of an activated state in macrophages and T cells, as demonstrated in an immunocompetent setting with spatial transcriptomics. Together, our data highlight the therapeutic promise of simultaneously targeting FACT and BET proteins in DMG, offering a dual tumor-intrinsic and immune-mediated strategy for combating this devastating pediatric brain tumor. - Source: PubMed
Publication date: 2026/01/14
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