Polyclonal SSRP1, Full length
- Known as:
- Polyclonal SSRP1, length
- Catalog number:
- pc-204
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal SSRP1 Full length
Related genes to: Polyclonal SSRP1, Full length
- 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: Polyclonal SSRP1, Full length
Related articles to: Polyclonal SSRP1, Full length
- Colorectal cancer (CRC) progression from benign polyps to malignant adenocarcinomas is a complex process involving the abnormal proliferation and differentiation of colon epithelial cells. Colorectal adenomas (CRAs), the precursors to most CRCs, are histologically classified into tubular adenomas (TAs), tubulovillous adenomas (TVAs), and villous adenomas (VAs). Despite new findings, the molecular signatures and pathways specific to each adenoma type remain poorly understood. This study aimed to identify specific biomarkers and pathways associated with the progression of TA, TVA, and VA to CRC. - Source: PubMed
Publication date: 2026/07/28
Kolour Haniye RahimiSarirchi SomayehZamani BaharehDaskar-Abkenar ElaheLooha Mehdi AzizmohammadZafarjafarzadeh NiktaKetabimoghadam PardisParvizi MaryamSadeghi AmirNobili StefaniaFatemi NayeralsadatMojarad Ehsan Nazemalhosseini - We recently identified the FACT-ETS-1 Antiviral Response (FEAR) pathway as an interferon-independent innate immune response that restricts DNA virus replication and that is antagonized by poxvirus-encoded A51R proteins (Rex et al., 2024, Nature Microbiology). The human FEAR pathway is mediated by the FACT complex, consisting of hSpt16 and SSRP1 subunits, that remodels chromatin to activate expression of the antiviral transcription factor, ETS-1. To counter this pathway, poxvirus A51R proteins tether SUMOylated hSpt16 subunits to microtubules to prevent ETS-1 expression. While these observations indicate a role for the FEAR pathway in DNA virus restriction, it was unclear if RNA viruses interact with this pathway. Here, we show that the RNA virus, vesicular stomatitis virus (VSV; Rhabdoviridae), is also restricted by the FEAR pathway but has evolved a distinct mechanism to block this antiviral response. Through in vitro assays and cell culture studies, we demonstrate that the VSV encoded matrix (M) protein directly interacts with SUMOylated hSpt16 to promote its ubiquitination and proteasome-dependent degradation. Using deletion mapping, we discovered a N-terminal motif in VSV M that is both required for interaction with host hSpt16 proteins and for their proteasomal degradation. This degradation effectively blocks ETS-1 induction and suppresses FEAR pathway activation during infection. Strains encoding mutant M proteins that cannot antagonize the FEAR pathway exhibit replication defects in human cells that can be rescued by hSpt16 or ETS-1 depletion, suggesting FEAR pathway evasion is critical for efficient VSV replication. Moreover, we show that the inability of VSV M to interact with and degrade SUMOylated Spt16 in lepidopteran cells results in an abortive infection, suggesting VSV-Spt16 interactions can influence virus host range. Collectively, our study illustrates that DNA and RNA viruses have independently evolved diverse mechanisms to antagonize SUMOylated host Spt16 proteins, underscoring the physiological importance of the FEAR pathway to antiviral immunity. - Source: PubMed
Publication date: 2026/07/17
Rex Emily ASeo DaheeEmbry AaronAlto Neal MGammon Don B - Facilitates chromatin transcription (FACT) is an evolutionarily conserved chromatin remodeling factor. It controls chromatin states in an ATP-independent manner via the regulation of chromatin assembly and disassembly. Through such regulation, FACT is involved in controlling transcription and other DNA-transacting processes such as replication and repair. However, it is surprisingly found to be upregulated in various cancers, and upregulated FACT induces oncogenesis and supports cancer cell survival, aggressiveness and metastasis, thus implying it to be a prognostic marker for cancer with an attractive targeted therapeutic potential. Here, we describe the involvement of FACT in various cancers with mechanistic insights and potential targeted therapeutic implications. - Source: PubMed
Publication date: 2026/06/08
Barman PriyankaBhaumik Sukesh R - 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