CMV ICP22 Monoclonal Antibody
- Known as:
- cytomegalovirus ICP22 Monoclonal Antibody
- Catalog number:
- CA0101
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Viagen
- Gene target:
- CMV ICP22 Monoclonal Antibody
Related genes to: CMV ICP22 Monoclonal Antibody
- Gene:
- MCRS1 NIH gene
- Name:
- microspherule protein 1
- Previous symbol:
- -
- Synonyms:
- ICP22BP, MSP58, P78, MCRS2, INO80Q
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-14
- Date modifiied:
- 2014-11-19
Related products to: CMV ICP22 Monoclonal Antibody
Related articles to: CMV ICP22 Monoclonal Antibody
- Branchio-oto-renal (BOR) syndrome is an autosomal dominant condition characterized by variable malformations including hearing loss and renal dysfunction. Variants in SIX1 or its activating co-factor EYA1 are causative in about 50% of patients. Some patients carrying BOR variants also present with craniosynostosis, indicating that cranial skeletal dysmorphologies could be an under-diagnosed feature. To date, most studies on the role of SIX1 have focused on its role in the cranial placode-based development of the inner ear, whereas its role in the neural crest cells of the mandibular arch, which will give rise to the jaws and middle ear ossicles, is less well characterized. Here, we present novel expression profiles of three putative SIX1 co-factors (PA2G4, MCRS1, and SOBP) in the developing mouse first pharyngeal arch and tooth. SIX1 colocalizes with PA2G4, MCRS1, and SOBP within the oral domain of the mandibular arch and during odontogenesis, although each exhibits a distinct expression pattern. Functional analyses revealed that SOBP binds SIX1, EYA1, and EYA2 and represses both SIX1 + EYA1 and SIX1 + EYA2 transcriptional activity, whereas MCRS1 binds only SIX1 and selectively represses SIX1 + EYA2 activity. In contrast, PA2G4 does not bind SIX1, yet modulates SIX1 + EYA2 activity. We further show that SIX1 is required for proper expression of Pa2g4, Mcrs1, and Sobp in the mouse mandibular arch. Collectively, these results demonstrate that regulation of SIX1 + EYA transcriptional activity is highly context dependent, occurs through both direct and indirect mechanisms, and differs between SIX1 + EYA1 and SIX1 + EYA2 complexes. These findings reveal species-specific differences and uncover a level of regulatory complexity not previously identified in Xenopus studies. - Source: PubMed
Publication date: 2026/07/16
Jourdeuil KarynChukwuocha KelechiGafurova JasminaBen-Mayor AshleyMoody Sally ATavares Andre L P - Aging and metabolic syndrome (MetS) are intertwined risk factors for breast cancer (BC), but the core molecular nexus integrating these states is unknown. This study aimed to identify and validate a causal driver at this intersection. - Source: PubMed
Publication date: 2026/01/20
Tao YiyingDing XibingXuan WeiZhu HaoLiu XiaohuaChen YuqingWu JialinDu JingTian JieQian Guojun - Pan-cancer analyses focused on the immunological significance and therapeutic potential of microspherule protein 1 (MCRS1) remain unreported. This study aims to define the pan-cancer immunological significance and therapeutic potential of MCRS1, with focused mechanistic dissection of its epigenetic-driven roles in hepatocellular carcinoma (HCC) progression. - Source: PubMed
Publication date: 2025/11/26
Wang QiangYe YuntaoZhang MengyuLi Bo - The evolutionarily conserved microspherule protein 1 (MCRS1) has diverse functions, ranging from transcriptional regulation to stabilization of microtubule minus ends in acentrosomal spindles in mammals. A previous study suggested that in the model plant Arabidopsis thaliana, inactivation of an MCRS1 homolog gene led to aborted embryogenesis. To test whether this lethality was caused solely by sporophytic defects, we used the heterozygous emb1967-1/mcrs1-1 mutant for reciprocal crosses with the wild-type plant and found that the MCRS1 gene was dispensable for the development of both male and female gametophytes. An MCRS1-GFP fusion protein was expressed in the mcrs1 mutant and suppressed the mutation as evidenced by restored growth. This functional fusion protein exclusively localized to interphase nuclei and became unnoticeable during mitosis before reappearing in the reforming daughter nuclei. Affinity purification of the MCRS1-GFP protein specifically recovered the Myb-like transcription factor DRMY1 (Development Regulated Myb-like 1) but not microtubule-associated factors. Direct MCRS1-DRMY1 interaction was also demonstrated by a localization-based assay in living cells. Thus, we hypothesized that MCRS1's function was perhaps linked to transcription factors like DRMY1 and its paralog DP1 for regulation of gene expression during sporophyte development. - Source: PubMed
Huo Huan HowardLuo MingLee Yuh-Ru JulieLiu Bo - Dampened antigen presentation underscores the resistance of pancreatic cancer to T cell-mediated anti-tumor immunity, rendering immunotherapy largely ineffective. By high-throughput CRISPR activation perturbation, we discovered that the transcriptional regulator MCRS1 significantly augmented the sensitivity of mouse pancreatic cancer cells to T cell immunity in vitro and in vivo. Mechanistically, MCRS1 interacted with the transcription factor and genome organizer YY1 to coordinately increase the chromatin accessibility and expression of MHC-I genes. Elevated MCRS1 subverted MHC-I suppression and activated anti-tumor T cells, which sensitized mouse pancreatic cancer to α-PD-1 therapy. Remarkably, high MCRS1 expression was associated with increased T cell infiltration and extended survival of patients with pancreatic cancer and was predictive of favorable responses to α-PD-1 therapy in patients with lung cancer. Together, our study uncovers that MCRS1 sensitizes cancer cells to T cell immunity by transcriptionally subverting MHC-I suppression, which enhances the effectiveness of α-PD-1 therapy in mice and humans, paving the way to further improve immunotherapy against solid tumors. - Source: PubMed
Publication date: 2024/11/15
Li XueYi HanJin ZheyuJiang KaitaoXue KangkangWang JinQian YupingXiang QianZhu SijingYan RunheYang YulongSun ShenfeiLi KaiZhou ZichuYu WeiJiang NingDing ChenLin XinhuaZhong JiangDong YuchaoLiu YanfangYu Xiaofei