Rat Anti-Mouse B220 (CD45R)
- Known as:
- Rat Antibody toMouse B220 (CD45R)
- Catalog number:
- 128-10005-1
- Product Quantity:
- 500
- 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)
- The Thanatos-associated (THAP) protein family, named after the Greek god of death, comprises zinc-finger proteins characterized by a DNA-binding domain called the THAP domain. Although THAP1 and THAP11 have been extensively studied, the broader family of twelve human THAP-domain containing proteins is increasingly recognized as an important but underexplored group of transcriptional regulators. Evidence now links THAP proteins to a wide range of cellular processes, including cell-cycle progression, DNA repair, apoptosis, proteostasis, and mitochondrial function. Dysregulation of these proteins has also been implicated in cancer and neurological disorders, underscoring their medical relevance. In this review, we summarize current knowledge of their structure, localization, transcriptional roles, and disease associations. We also present new structural analyses that shed light on conserved and divergent features across the THAP family. Finally, we will highlight their newly appreciated functions in stem and progenitor cell biology. - Source: PubMed
Publication date: 2026/07/08
Rampal BryceBrisson AlexandreBen Hamou Kuijpers LouiseCappadocia LaurentSamarut Éric - Expanded short tandem repeats contribute to a broad spectrum of neurodegenerative diseases, yet their roles in Parkinson's disease (PD) and parkinsonism remain incompletely characterized, especially across diverse ancestries. We analyzed short-read whole-genome (WGS) and clinical exome sequencing (CES) data from 38,365 individuals (28,861 WGS; 9,504 CES), encompassing 23,242 patients with PD, 4,729 patients with atypical parkinsonism and 10,394 healthy controls from 11 genetic ancestries. To determine carrier frequencies and characterize repeat structures across diverse ancestries, we genotyped 12 established pathogenic loci where normal, intermediate, and pathogenic alleles can be reliably differentiated using short-read sequencing data. Additionally, we conducted threshold-based associations to determine the minimum threshold associated with increased PD risk in 15,995 individuals (8,591 PD, 7,404 controls) of European ancestry. Pathogenic repeat expansions were detected in 62 patients (56 PD and 6 atypical parkinsonism) and 5 controls across seven loci ( and ), spanning seven ancestries. Among these, expansions were the most frequently observed in PD and were present in African, East Asian, European and Middle Eastern ancestries. Additionally, intermediate repeat expansions exhibited a strong, length-dependent association with PD risk in the European population, with individuals with ≥32 repeats having a more than four-fold increased risk (odds ratio 4.25, 95% confidence interval 1.80-12.05). Overall, >92% of expanded alleles harbor CAA interruptions within the CAG tract. Pathogenic expansions at other loci, such as and , showed more ancestry-specific distributions. Clinically, individuals with pathogenic and expansions most often presented with typical PD features but frequently showed earlier disease onset and a strong family history of PD. This large-scale, multi-ancestry study comprehensively maps the genetic landscape of pathogenic and intermediate repeat expansions in PD. Our findings confirm a length- and structure-dependent risk association for with PD in the European population and highlight the pleiotropic effects of repeat expansions across the parkinsonian spectrum. - Source: PubMed
Publication date: 2026/06/22
Lange Lara MCerquera-Cleves CatalinaTan Ai HueyLim Shen-YangOkubadejo Njideka ULin Chin-HsienChen Pin-ShiuanShin Jung HwanAhmad-Annuar AzlinaScreven Laurel AChelban VioricaDilliot Allison AFienemann AndréGalvelis Kamalini GhoshHoulden HenryIwaki HirotakaJaunmuktane ZaneCullinane Patrick WWarner ThomasJunker JohannaKanana YuliiaSarmiento Ignacio J KellerKlein ChristineKung Pin-JuiLeonard Hampton LMencacci Niccoló ENalls Mike AReal RaquelSassi Samia BenTrinh JoanneVitale DanWestenberger AnaWu Lesley YSingleton Andrew BMorris Huw RLohmann KatjaBlauwendraat CornelisHeutink PeterFang Zih-Hua - Acute myeloid leukemia (AML) is a heterogeneous malignancy with frequent relapse, driven by intertwined alterations in mitochondrial function, cell cycle control, genome maintenance, and immune evasion. DDX28 is a mitochondrial DEAD-box RNA helicase required for mitoribosome assembly and mitochondrial translation, and has been implicated in bioenergetic regulation in other tumor contexts. Here, we profiled DDX28 expression across AML cohorts using integrated multi-omics resources and evaluated its associations with prognosis, immune microenvironment features, and predicted drug response. Functional annotation, pathway analysis, GSEA, and targeted in vitro assays were used to explore potential mechanisms. High DDX28 expression was associated with inferior survival and higher blast burden. Mechanistically, elevated DDX28 expression was linked to promoter hypomethylation and was positively correlated with the transcription factor THAP11. Transcriptomic signatures in the high DDX28 group were enriched for cell cycle progression and DNA damage repair programs, together with an immune-suppressive landscape characterized by increased regulatory T cells and M2 macrophage signatures. Single-cell RNA-seq analyses further showed DDX28 enrichment in malignant blasts and exhausted or proliferative T-cell states. Consistently, DDX28 knockdown by siRNA in HEL cells reduced proliferation and impaired migration and invasion. Although direct metabolic flux measurements were not performed, the mitochondrial localization of DDX28 and the enrichment of proliferation and repair programs support a model in which DDX28 couples mitochondrial translation with the biosynthetic and genome maintenance demands of rapidly cycling AML cells. Collectively, our findings identify DDX28 as a prognostic indicator and a candidate regulator of malignant and immune states in AML, with potential relevance to therapeutic response. - Source: PubMed
Publication date: 2026/05/05
Wang ZiLiu YunliGuan XinzhuYe MiaoqingXu Xinxin - 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