MOSC1 Blocking Peptide
- Known as:
- MOSC1 Blocking Peptide
- Catalog number:
- 33r-9937
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- MOSC1 Blocking Peptide
Related genes to: MOSC1 Blocking Peptide
- Gene:
- MARC1 NIH gene
- Name:
- mitochondrial amidoxime reducing component 1
- Previous symbol:
- MOSC1
- Synonyms:
- FLJ22390
- Chromosome:
- 1q41
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-03
- Date modifiied:
- 2017-02-01
Related products to: MOSC1 Blocking Peptide
Related articles to: MOSC1 Blocking Peptide
- We present REMAP (Recording Evolution in Mammary tumors via Active PyMT), a lineage-tracing mouse model that integrates inducible CRISPR recording with the MMTV-PyMT model of hormone receptor-positive (HR+) breast cancer. Inducible Cas9 drives editing of MARC1 homing guide RNAs (hgRNAs), generating heritable lineage marks, and enables reconstruction of clonal relationships. Using REMAP, we profiled tumor evolution and response to radiation combined with anti-PD1 immunotherapy. Treatment reduced tumor burden locally and systemically, and single-cell RNA sequencing revealed remodeling of the tumor microenvironment (TME). We identified metastatic clones present across primary tumors and distant sites, which exhibited elevated epithelial-mesenchymal transition (EMT) programs as a heritable clonal state. Treatment reduced EMT-associated transcriptional programs and reshaped immune composition, with radiation driving clonal expansion of T cells and reduced repertoire diversity. In contrast, cancer-associated fibroblast clones spanned multiple transcriptional states, indicating substantial stromal plasticity. Together, REMAP enables high-resolution coupling of clonal history and cellular state in vivo, revealing that tumor progression, metastasis, and therapeutic response are governed by heritable lineage programs. - Source: PubMed
Publication date: 2026/04/18
Marshall Abigail CVahey JackieBagheri MeisamSaxe RachelFields JenniferKolling FredMcKenna Aaron - Metabolic dysfunction-associated steatotic liver disease (MASLD) spans from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) and can progress to cirrhosis or hepatocellular carcinoma. Despite its prevalence, effective therapies are lacking. Recent genome-wide association studies identified a common missense variant (rs2642438) in the Mitochondrial Amidoxime Reducing Component 1 (MTARC1) gene that protects against liver cirrhosis without increasing cardiovascular disease risk. Biochemical and disease risk signatures associated with carriers of this missense variant also aligned with those of a known loss-of-function MTARC1 variant, suggesting mARC1 inhibition as a potential MASLD treatment. - Source: PubMed
Yin XiaofeiBickerton CarolineMacDonald BryanArduini AlessandroShi YunlongHaas MaryDeik AmyChaffin MarkKovacs-Bogdan ErikaPacheco Julian AvilaAmegadjie MaiwenBhandary BidurSadre ShayanRathjen ThomasPapangeli IrinnaChung Raymond TGoodman RussellClaussnitzer MelinaClish ClaryEhrmann AlexanderLeed AlisonEllinor Patrick T - Metabolic dysfunction-associated steatotic liver disease (MASLD) is a disorder characterized by anomalous hepatic fat accumulation and one of the leading causes of chronic liver disease. Recent genome-wide association studies identified a missense variant (p.A165T) in the gene encoding mitochondrial amidoxime-reducing component 1 (mARC1) that is strongly associated with protection against MASLD, cirrhosis, and liver-related mortality; however, the mechanism of this protective effect remains unknown. Recent reports have demonstrated that both global genetic deletion and hepatocyte-specific knockdown of mARC1 significantly attenuate liver steatosis and fibrosis in multiple mouse models of diet-induced metabolic dysfunction-associated steatohepatitis (MASH). In this study, we generated the first genetically engineered mouse model with a mARC1 A168T amino acid substitution, the murine ortholog of the human mARC1 A165T variant, and evaluated the impact of this substitution in multiple mouse models of MASH and liver fibrosis; additionally, we sought to characterize the sexual dimorphism of this mARC1 amino acid substitution in MASLD pathology. Profiling of expression levels across mouse tissues revealed that mARC1 protein levels were significantly reduced while messenger RNA (mRNA) expression was not affected in mARC1 A168T mice. While female mice were more resistant to the effects of diet-induced MASH than males, neither female nor male A168T mice showed significantly reduced liver steatosis, inflammation, or fibrosis in multiple models of MASH and liver fibrosis. We have demonstrated that an A168T substitution within the mARC1 protein is not sufficient to protect mice from the deleterious effects of MASH, and further investigation of the functional consequences of this variant is required. - Source: PubMed
Pandovski SentibelYang TiffanyZhou HeatherRosahl Thomas WCarballo-Jane EsterTalukdar SaswataCoyne Erin S - Understanding the genetic mechanism of cold adaptation in cashmere goats and dairy goats is very important to improve their production performance. The purpose of this study was to comprehensively analyze the genetic basis of goat adaptation to cold environments, clarify the impact of environmental factors on genome diversity, and lay the foundation for breeding goat breeds to adapt to climate change. A total of 240 dairy goats were subjected to genome resequencing, and the whole genome sequencing data of 57 individuals from 6 published breeds were incorporated. By integrating multiple approaches such as phylogenetic analysis, population structure analysis, gene flow and population history exploration, selection signal analysis, and genome-environment association analysis, an in-depth investigation was carried out. Phylogenetic analysis unraveled the genetic relationships and differentiation patterns among dairy goats and other goat breeds. Through signal analysis (θπ, FST, XP-CLR), we identified numerous candidate genes associated with cold adaptation in dairy goats (STRIP1, ALX3, HTR4, NTRK2, MRPL11, PELI3, DPP3, BBS1) and cashmere goats (MED12L, MARC2, MARC1, DSG3, C6H4orf22, CHD7, MYPN, KIAA0825, MITF). Genome-environment association (GEA) analysis confirmed the link between these genes and environmental factors. Moreover, a detailed analysis of the critical genes C6H4orf22 and STRIP1 demonstrated their significant roles in the geographical variations of cold adaptation and allele frequency differences among different breeds. This study contributes to understanding the genetic basis of cold adaptation, providing crucial theoretical support for precision breeding programs aimed at improving production performance in cold regions by leveraging adaptive alleles, thereby ensuring sustainable animal husbandry. - Source: PubMed
Publication date: 2025/09/09
Zhao JianqingYao WeiweiLiu QingqingGong PingMu YuanpanWang WeiLiu BaolongLi CongShi HengboLuo Jun - - Source: PubMed
Publication date: 2025/08/06
Xu JianZhang WeiWu GuoLi Jingdong