BCL11B Antibody - C-terminal region (ARP33294_P050)
- Known as:
- BCL11B Antibody - C-terminal region (ARP33294_P050)
- Catalog number:
- arp33294_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- BCL11B Antibody - C-terminal region (ARP33294_P050)
Related genes to: BCL11B Antibody - C-terminal region (ARP33294_P050)
- Gene:
- BCL11B NIH gene
- Name:
- BAF chromatin remodeling complex subunit BCL11B
- Previous symbol:
- ZNF856B
- Synonyms:
- CTIP-2, CTIP2, hRIT1-alpha
- Chromosome:
- 14q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-28
- Date modifiied:
- 2019-01-25
Related products to: BCL11B Antibody - C-terminal region (ARP33294_P050)
Related articles to: BCL11B Antibody - C-terminal region (ARP33294_P050)
- The guinea fowl (), a thermo-tolerant and disease-resilient poultry species, holds great potential for sustainable poultry production in climate-vulnerable regions. The genomic aspects of this species remain largely understudied. The present study aims to delineate the patterns of domestication and understand the evolutionary dynamics of guinea fowl populations (wild and domestic) across three continents, utilizing whole-genome sequencing data from 122 genomes. The population structure analyses (ADMIXTURE, PCA, phylogeny, F, LD, and MAF) revealed that Indian guinea fowl (CARI) shared close ancestry with Iranian (IRAD) and Chinese (CHID) domesticated populations while remaining distinct from wild lineages. The runs of homozygosity (ROH) identified 49,088 segments, with short fragments (ROHs) preponderant in Indian and domestic populations, reflecting historical inbreeding and effects of domestication cum selection. Copy number variation (CNV) analysis revealed 105,178 CNVs concatenated into 40,067 CNV regions (CNVRs) across 11 populations, establishing the first CNV atlas for guinea fowl at the global level. Gene annotation of overlapping ROH and CNVRs revealed 1080 common candidates across Asian guinea fowl populations, i.e., the Indian guinea fowl (CARI), IRAD, and CHID, including , , , and . These genes have earlier been associated with immune regulation, stress response, and thermal adaptation. Selection signature scans, integrating intra-population (iHS) and inter-population (XP-EHH) approaches, uncovered genes under positive selection linked to immune response (like , , and ), thermo-tolerance (like and ), lipid metabolism (like and ), and pigmentation (). These signatures highlight the molecular basis of resilience in guinea fowl and their potential to withstand climate-induced stresses. This study presents the first global CNV atlas for guinea fowl and provides the first comprehensive genomic characterization of the Indian domestic population, integrating ROH, CNV, and selection signature analyses. It offers a comprehensive assessment of guinea fowl genomes (wild and domesticated) across three continents, offering insights into domestication, evolutionary dynamics, and the genetic basis of their adaptation and resilience. - Source: PubMed
Publication date: 2026/03/25
Tomar SimmiAhmad Sheikh FirdousGangwar MunishAzhaguraja ManoharanKush AlishaTrivedi AbhaGandham Ravi KumarTiwari Ashok Kumar - - Source: PubMed
Publication date: 2026/04/02
Magocova VeronikaSvorenova TatianaHan VladimirBánoci JanKaťuch VladimírKollova AureliaKnorovsky KamilOstrozovicova MiriamZech MichaelSkorvanek Matej - Suboptimal glycemic control facilitates tumor immune evasion, severely impairing the prognosis of patients with cancer. Tumor cell softness, a critical biomechanical property, is closely associated with cell proliferation, migration, and immune cell interactions, thereby regulating tumor progression. However, whether blood glucose induces immune evasion by modulating tumor cell hardness-defined as a "physical property immune checkpoint"-and its underlying mechanisms remain unclear. This study demonstrates that elevated glucose concentrations in culture systems progressively soften tumor cells, reducing the cytotoxicity of CD8 T cells. Specifically, glucose increases cytoplasmic and plasma membrane cholesterol levels in tumor cells, reducing cellular hardness. Mechanistically, hyperglycemia disrupts DNA methylation in tumor cells: dysregulated expression of DNA methyltransferase DNMT3A and demethylase TET2 enhances methylation of the cholesterol efflux gene ABCA1 promoter, downregulating ABCA1. Impaired ABCA1 hinders cholesterol efflux, causing intracellular accumulation, increasing plasma membrane cholesterol, softening cells, and weakening T-cell cytotoxicity. Additionally, BCL11B binds the ABCA1 promoter, recruiting DNMT3A and TET2 to regulate methylation. In conclusion, this study identifies glucose-mediated modulation of the tumor cell membrane-force axis in immune evasion, clarifies the links between hyperglycemia-induced DNA methylation dysregulation, aberrant cholesterol accumulation and the cell hardness, contributing to the poor prognosis of cancer patients with suboptimal glycemic control from a biomechanical perspective. - Source: PubMed
Publication date: 2026/03/24
Yang ChengMei RuiyanLiu JingyiShen XiangjingZhang HaihuaLi QianGan DongxueShi JingjieYang RuiZhao YanLu YiyangLi HongWang KairuiLi JunqiangSu Haichuan - Fanconi anemia (FA) is a genetic disorder typically characterized by progressive bone marrow failure (BMF) during childhood, leading to diagnosis at that stage. In adolescence or adulthood, patients are predisposed to myelodysplastic syndrome (MDS), acute myeloid leukemia, and solid tumors. However, some individuals present atypically, delaying FA recognition and resulting in life-threatening complications. This study describes the distinctive phenotype associated with biallelic pathogenic variants. - Source: PubMed
Publication date: 2026/03/25
Pegoraro FrancescoLarcher LiseKim RathanaPagès MélaniePasset MarieCaye-Eude AurélieFahd MonyBrethon BenoitHernandez LucieVasquez NadiaDa Costa MélanieAuger NathalieLachaud Christophede Tersant MarieLuporsi ElisabethSébert MarieDalle Jean-HuguesPeffault de Latour RégisClappier EmmanuelleStoppa-Lyonnet DominiqueLeblanc ThierryPaillard CatherineSicre de Fontbrune FloreSoulier Jean - In this study, we used optical genome mapping (OGM), conventional karyotyping, and next-generation sequencing to analyze cytogenomic alterations in 91 cases of T-cell acute lymphoblastic leukemia/lymphoma (T-ALL). Whereas karyotyping detected abnormal karyotypes in 55% of cases, OGM identified cytogenetic abnormalities in 97.8% of the cases and provided clinically relevant information beyond karyotyping in ∼70% of cases. OGM detected gene rearrangements in 80% of cases, including 24 recurrent gene fusions and 21 previously unreported putative gene fusions in T-ALL. Copy number variants were detected in 93% of cases, with interstitial deletions the most common. Gene mutations were detected in 93% of cases, with NOTCH1 being most frequent (in 57% of cases). Combining all data, most T-ALL cases harbored 3 or more cytogenomic aberrations. Specific cytogenomic alterations differed among T-ALL subtypes as follows: rearrangements of BCL11B and PICALM::MLLT10, deletions of 7p, and mutations involving DNMT3A, WT1, TET2, IDH2, and FLT3 were common in early T-precursor and near-early T-precursor subtypes. Rearrangements of TLX1, KMT2A, STIL::TAL1, and NUP214::ABL1, deletions of 9p, and FBXW7 mutations were frequently associated with the cortical subtype. We conclude that integration of OGM and next-generation sequencing with karyotyping enables comprehensive cytogenomic profiling of T-ALL that improves detection of clinically relevant genomic alterations and may inform disease classification and future studies of risk stratification. - Source: PubMed
Publication date: 2026/03/06
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