MGC33926 Blocking Peptide
- Known as:
- MGC33926 Blocking Peptide
- Catalog number:
- 33r-8049
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- MGC33926 Blocking Peptide
Related genes to: MGC33926 Blocking Peptide
- Gene:
- TMEM178A NIH gene
- Name:
- transmembrane protein 178A
- Previous symbol:
- TMEM178
- Synonyms:
- MGC33926
- Chromosome:
- 2p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-18
- Date modifiied:
- 2014-11-19
Related products to: MGC33926 Blocking Peptide
Related articles to: MGC33926 Blocking Peptide
- Antiretroviral therapy (ART) has transformed HIV from a fatal disease into manageable circumstance. However, the HIV reservoirs remain a main barrier to complete cure. This review emphasized when, where and how the latency is established, with focus on various host factors and viral proteins. We highlight the importance of Tat and Rev in facilitating the export and stability of HIV latency. We discuss how transcription factors such as NFκB, NFAT, and Sp1 regulate HIV gene expression during T cell activation, while other factors like MRTFB, BACH2, FOXO1, HMGB1, SAMHD1, APOBEC3, TRIM5, Wnt/β-catenin and LEDGF/p75 also contribute to the persistence of reservoirs. Recent studies have also identified novel restriction and immune regulatory factors such as, LAPTM5, KRT72, and CARD8, directly or indirectly influencing HIV 1 latency. The advancements in CRISPR screening technology have also identified novel host factors, such as FBXO34, FTSJ3, TMEM178A, NICN1, PEBP1, ZNF304 and ORC1, that are associated with HIV-1 latency. These findings underscore the multifaceted nature of viral latency and ongoing need for research to develop effective strategies for viral eradication. - Source: PubMed
Publication date: 2025/05/20
Yang ChenboTong LingXue Jing - Immune checkpoint inhibitor (ICI) therapy has proven to be a promising treatment for colorectal cancer (CRC). We aim to investigate the relationship between DNA methylation and tumor mutation burden (TMB) by integrating genomic and epigenetic profiles to precisely identify clinical benefit populations and to evaluate the effect of ICI therapy. - Source: PubMed
Publication date: 2023/01/13
Huang HaoCao WeifanLong ZhipingKuang LeiLi XiFeng YifeiWu YuyingZhao YangChen YinggangSun PengPeng PanxinZhang JinliYuan LijunLi TianzeHu HuifangLi GairuiYang LongkunZhang XingHu FulanSun XizhuoHu Dongsheng - To counter HIV latency, it is important to develop a better understanding of the full range of host factors promoting latency. Their identification could suggest new strategies to reactivate latent proviruses and subsequently kill the host cells ("shock and kill"), or to permanently silence these latent proviruses ("block and lock"). We recently developed a screening strategy termed "Reiterative Enrichment and Authentication of CRISPRi Targets" (REACT) that can unambiguously identify host genes promoting HIV latency, even in the presence of high background "noise" produced by the stochastic nature of HIV reactivation. After applying this strategy in four cell lines displaying different levels of HIV inducibility, we identified FTSJ3, TMEM178A, NICN1 and the Integrator Complex as host genes promoting HIV latency. shRNA knockdown of these four repressive factors significantly enhances HIV expression in primary CD4 T cells, and active HIV infection is preferentially found in cells expressing lower levels of these four factors. Mechanistically, we found that downregulation of these newly identified host inhibitors stimulates different stages of RNA Polymerase II-mediated transcription of HIV-1. The identification and validation of these new host inhibitors provide insight into the novel mechanisms that maintain HIV latency even when cells are activated and undergo cell division. - Source: PubMed
Publication date: 2020/12/03
Li ZichongHajian CyrusGreene Warner C