Rat Anti-Mouse B220 (CD45R)
- Known as:
- Rat Antibody toMouse B220 (CD45R)
- Catalog number:
- 128-10005-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse B220 (CD45R)
Related genes to: Rat Anti-Mouse B220 (CD45R)
- Gene:
- THAP11 NIH gene
- Name:
- THAP domain containing 11
- Previous symbol:
- -
- Synonyms:
- HRIHFB2206, CTG-B45d, CTG-B43a
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-08
- Date modifiied:
- 2015-08-26
Related products to: Rat Anti-Mouse B220 (CD45R)
Related articles to: Rat Anti-Mouse B220 (CD45R)
- Differentiation of trophoblast stem (TS) cells or progenitor cytotrophoblasts (CTBs) into multinucleated syncytiotrophoblasts (STBs) is essential for placental development. Disruption of this process contributes to major obstetrical syndromes, including fetal growth restriction and preeclampsia, and Trisomy 21. However, the chromatin mechanisms governing trophoblast stemness and differentiation remain inadequately defined. Here we identify the chromatin-associated factor PHF13, uncovered through a high-throughput microRNA target screen, as a key regulator of trophoblast cell fate. PHF13 knockout TS cells exhibited defects that ultimately resulted in loss of cell viability, whereas PHF13 knockdown promoted expression of fusion-associated genes, including ERVFRD-1 and human chorionic gonadotropin (hCG). Consistently, PHF13 depletion in BeWo trophoblast cells increased hCG expression and secretion while reducing expression of canonical stemness-associated transcription factors ELF5 and TEAD4. Integrated genomic analyses further revealed that PHF13 target genes comprise a gene regulatory network that maintains trophoblast stemness and restrains differentiation. Notably, the pluripotency-associated transcription factor THAP11 partially co-occupies genomic sites with PHF13. Together, these findings establish PHF13 as a previously unrecognized chromatin regulator of trophoblast stemness and differentiation, providing mechanistic insight into pathways critical for placental development and function. - Source: PubMed
Publication date: 2026/03/17
Liu ShengLiu LeiMeng JiayuSadovsky ElenaHuang KeyiSorenson HeatherChu TianjiaoSadovsky YoelOuyang Yingshi - Spinocerebellar ataxia (SCA) type 51 is a neurodegenerative disease caused by CAG repeat expansions in exon 1 of the THAP11 gene. These repeats are translated into a glutamine-rich protein, THAP11-polyQ, which forms protein aggregates and exhibits toxicity in cell models; however, the underlying mechanism remains unclear. In this study, we generate transgenic Drosophila models expressing varying lengths of THAP11-polyQ using the UAS-GAL4 system and assess neurodegeneration through pathological and behavioral analyses. Our results demonstrate that expression of THAP11-polyQ in transgenic flies leads to progressive neuronal cell loss, locomotor deficiency, and reduced survival. RNA sequencing of patient-derived skin fibroblasts reveals significant enrichment of the PI3K-Akt-mTOR pathway, and electron microscopy of transgenic flies shows an increase in multilamellar bodies, suggesting involvement of autophagy in SCA51. Consequently, we treat the fly model with rapamycin, an mTOR inhibitor known to enhance autophagy. This treatment reduces toxic THAP11-polyQ protein aggregates, significantly alleviates neuronal degeneration, and improves locomotor function, consistent with the rescue effects observed upon overexpression of Atg8a. Overall, these findings suggest that the Drosophila model, which recapitulates the neurodegenerative features of SCA51, can be used to investigate pathogenic mechanisms and that rapamycin holds promising potential as a therapeutic approach for this disease. - Source: PubMed
Publication date: 2025/08/29
Wei CuijieJi TaoyunXu JinZheng YileiZheng FuzeWang SuxiaGao ChaoWan YalanLi ZhenyuDeng JianwenXiong Hui - The interplay between host innate immunity and pathogen evasion is a dynamic battle shaping infection outcomes. The Topical Collection "Regulation of Antiviral and Antimicrobial Innate Immunity and Immune Evasion" synthesizes findings from thirteen recent studies to elucidate the molecular mechanisms of innate immune signaling and pathogen countermeasures. Host pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and DNA sensor cyclic GMP-AMP synthase (cGAS), drive type I interferon (IFN-I) and interferon-stimulated genes (ISGs) responses, alongside processes like autophagy and inflammasome activation, to combat viral and bacterial infections. Pathogens, such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), cytomegalovirus, and porcine reproductive and respiratory syndrome virus, deploy sophisticated strategies to target immune sensors and adaptors, enabling replication and persistence. Novel insights, including the roles of ISG15, autophagy protein ATG7, and host factors such as THAP11 and PSMB4, highlight complex interactions influencing viral replication and host defense. These studies propose targeted therapeutic strategies, such as inflammasome modulation for human immunodeficiency viruses (HIV), and prostaglandin E2 regulation for foot-and-mouth disease virus vaccine production, offering promising avenues to enhance host immunity and counter pathogen evasion. - Source: PubMed
Publication date: 2025/08/29
Wang LingHe DandanSatoh-Takayama NaokoZheng ChunfuXing Junji - Porcine reproductive and respiratory syndrome virus (PRRSV) is a highly infectious pathogen in the global pig industry that causes significant economic losses. Owing to its rapid mutation, effective antiviral treatments or vaccines are still lacking. Therefore, it is essential to identify potential host factors that interact with PRRSV-encoded proteins. In this study, a porcine alveolar macrophage cDNA library was used to identify host proteins that interact with PRRSV nonstructural protein 1β (Nsp1β) via a yeast two-hybrid system. A total of 34 potential host factors were identified, with Thanatos-associated protein 11 (THAP11) strongly interacting with Nsp1β. These interactions were further analyzed via Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Co-localization of Nsp1β with THAP11, poly(rC)-binding protein 1 (PCBP1), thioredoxin-interacting protein (TXNIP), and cathepsin D (CTSD) was observed, and co-IP assays confirmed the Nsp1β-THAP11 interaction. The overexpression of THAP11 reduced PRRSV N protein accumulation, indicating an antiviral effect, whereas the silencing of THAP11 increased PRRSV replication. Furthermore, THAP11 promoted the degradation of Nsp1β by increasing K48- and K63-linked ubiquitination, thereby restricting PRRSV replication. These findings suggest that THAP11 exerts an antiviral effect by interacting with and degrading Nsp1β via the ubiquitin-proteasome system, providing insights for future PRRSV defence strategies. - Source: PubMed
Publication date: 2025/06/23
Chen BinghuaXie YongshengHe ZhanChen YongjieYan JiecongLi FangfangLuo YunyanPan YanfeiLiu MinGuo Chunhe - Less than half of the individuals with hereditary cerebellar ataxia receives a genetic diagnosis. Repeat expansions account for disproportionate number of hereditary cerebellar ataxia and have genetically heterogeneous causes. These genetic loci include , , , , , , , , , and This study aims to assess the yield of short-read whole genome sequencing in the molecular diagnosis of hereditary cerebellar ataxia. We recruited 380 patients (351 probands) from a national ataxia centre in United Kingdom. They underwent short-read whole genome sequencing as a part of the 100 000 Genomes Project. Bioinformatic pipeline of whole genome sequencing include variant prioritization in selected virtual gene panels, customized analysis with a focus on repeat expansions, structural variants and recently reported hereditary cerebellar ataxia genes. All potential genetic variants were reviewed in a multidisciplinary team, and further confirmation tests were performed as appropriate. Whole genome sequencing identified causative variants in 115 (33%) out of 351 probands. We established 46 distinct presumptive molecular diagnoses with the most frequent being ( = 22) ( = 20) and ( = 10). However, it failed to detect any probands with novel ataxia gene , which was subsequently identified on polymerase chain reaction screening in 10 unsolved probands. In conclusion, whole genome sequencing is a useful diagnostic test in hereditary cerebellar ataxia patients and can be used to detect repeat expansions, structural and mitochondrial variants. However, identification of complex structural variants and sizing of large repeat expansions remains a challenge and require alternative molecular testing techniques. - Source: PubMed
Publication date: 2025/05/17
Yau Wai YanSullivan RoisinO'Connor EmerPellerin DavidParkinson Michael HGiunti PaolaDicaire Marie-JoséeDanzi Matt CZüchner StephanBrais BernardWood Nicholas WHoulden HenryVandrovcova Jana