Pms1 siRNA_Lentivectors
- Known as:
- Pms1 siRNA_Lentivectors
- Catalog number:
- i064420a
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Pms1 siRNA_Lentivectors
Related genes to: Pms1 siRNA_Lentivectors
- Gene:
- PMS1 NIH gene
- Name:
- PMS1 homolog 1, mismatch repair system component
- Previous symbol:
- PMSL1
- Synonyms:
- MLH2
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2019-04-23
Related products to: Pms1 siRNA_Lentivectors
Related articles to: Pms1 siRNA_Lentivectors
- The incidence of early-onset colorectal cancer (EO-CRC; age <50 years) has been increasing worldwide. This single-center retrospective study aimed to compare the clinical characteristics of EO-CRC and late-onset CRC (LO-CRC; age ≥ 50 years) and to identify age-specific prognostic factors for overall survival (OS). - Source: PubMed
Publication date: 2026/07/01
Huang LifangZhong RuntaoLi KangkangChen JinfengHe YunxianYe YuanningChen ShuxianWei QiliMai HuizhenZhang YaliWang Zhiqing - Human and mouse genetics have established mismatch repair (MMR) as a central mediator of somatic repeat expansion, a key pathogenic process in Huntington's disease (HD) and related disorders. How individual MMR components function within the intact mammalian brain and interact with broader cellular networks remains poorly understood. We screened more than 500 chemically stabilized siRNAs targeting 10 MMR genes and used interventional RNAi in the Q111 HD mouse model to systematically dissect MMR function in vivo. MSH3 and PMS1 emerged as the most dose-sensitive regulators of somatic expansion but displayed markedly different effects on proteome stability. Quantitative proteomics generated an in vivo atlas of MMR component abundance and cross-regulation in the mammalian CNS, uncovering extensive connectivity between DNA repair, transcriptional regulation, chromatin remodeling, and mitochondrial biology. Together, these findings establish a systems-level framework linking MMR biology to neuronal function and offer mechanistic insight into selective neuronal vulnerability in HD. - Source: PubMed
Publication date: 2026/06/24
Belgrad JillianGreco Todd MSapp EllenSummers AshleyO'Reilly DanielLuu EricHutton Josiah EYamada NozomiFakih Hassan HFurgal RaymondEcheverria DimasMcHugh NicholasBramato BriannaFurguson ChantalHildebrand SamuelAllen SarahGaston NicholasCooper DavidMaebius AllisonGross Katherine YVogt Thomas FFinley MichaelPrasad BrindaDiFiglia MarianCristea Ileana MAronin NeilKhvorova Anastasia - Arsenic poisoning significantly elevates the risk of cancer and other chronic illnesses. The goal of this research is to identify important genes whose expression changes in response to arsenic toxicity, and the molecular pathways affected by arsenic, using computational analysis of arsenic toxicity profiles. This approach will computationally identify and analyze genes whose expression changes in response to arsenic, thereby elucidating the heightened risk of carcinogenesis in arsenic-exposed individuals. This work employed high-throughput arsenic toxicity profiles to computationally identify and analyze expressed genes (DEGs) differentially in Affymetrix microarray datasets from the Gene Expression Omnibus (GEO) database, which were screened using the GEO2R program. A protein-protein interaction (PPI) network was constructed using STRING to elucidate the functional links between these DEGs and DNA repair genes. Interactions between the seven central genes (E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS) and the repair genes PARP1, NBN, PMS1, MSH3, XRCC5, XRCC6, MGMT, and MLH1 were discovered. We employed the DAVID and Enrichr-KG platforms to investigate the functions of these genes and their associations with cellular and molecular processes in greater detail. Two hundred eighty-one non-synonymous single-nucleotide polymorphisms (nsSNPs) in the 07 genes linked to arsenic toxicity were found using the COSMIC database. Based on our analysis, mutations in E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS can hinder DNA repair mechanisms, ultimately leading to cancer. Our computational analysis demonstrated that these non-synonymous SNPs can affect gene function, potentially altering protein stability and activity. Furthermore, according to Metal-Protein docking and protein-protein docking, these genes and their mutations appear to affect interactions with repair proteins substantially. Specific dietary consumption may lessen the detrimental effects of arsenic poisoning on protein function. We hypothesized that the mutations might be reversed by attaching particular molecules to these mutants. The protective effects of six curcumin compounds were examined using molecular docking with AutoDock 4.2.6 to assess protein dynamics and binding interactions. Optimal complexes were selected for dynamics simulation using GROMACS, and potential strategies for long-term cancer prevention related to arsenic exposure were identified. - Source: PubMed
Parida LuckyPatel Trupti N - Pulmonary mixed neuroendocrine and non-neuroendocrine neoplasms (MiNENs) are currently described in the World Health Organization (WHO) classification primarily as combinations of non-small cell lung cancer (NSCLC) and high-grade neuroendocrine carcinomas, such as small cell lung cancer (SCLC) or large cell neuroendocrine carcinoma (LCNEC). The coexistence of NSCLC with typical or atypical carcinoid (TC/AC) tumors is not officially recognized in the current classification and remains an exceptionally rare entity, with limited information on its pathogenesis. We sought to delineate the molecular alterations underlying a rare case of MiNEN composed of AC and adenocarcinoma. - Source: PubMed
Publication date: 2026/03/19
Kim Kyoung MinKim Jong HunChung Myoung Ja - Bipolar disorder (BD) exhibits significant sex differences in its frequency, symptom presentation, and treatment response, suggesting distinct underlying neurobiological mechanisms. However, transcriptomic studies investigating these sex-specific pathways have been fragmented and underpowered. - Source: PubMed
Publication date: 2026/05/08
Davarinejad OmranMoradi Mohammad-TaherSafarzadeh ArashJalalvand MasumehKazemisafa Fatemeh