Ask about this productRelated genes to: Mbtd1 Blocking Peptide
- Gene:
- MBTD1 NIH gene
- Name:
- mbt domain containing 1
- Previous symbol:
- -
- Synonyms:
- SA49P01, FLJ20055
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-15
- Date modifiied:
- 2015-04-21
Related products to: Mbtd1 Blocking Peptide
Related articles to: Mbtd1 Blocking Peptide
- The emerging focus on epigenetic regulation in cancer biology has unveiled the significant role of CXorf67, a protein encoded by a gene on the X chromosome. CXorf67 interacts with core components of PRC2, namely EZH2 and SUZ12, thereby influencing histone modifications like H3K27me3. Research indicates that CXorf67 is overexpressed in specific malignancies, including posterior fossa ependymomas, diffuse midline glioma, endometrial stromal sarcoma, non-small cell lung cancer, and Merkel cell carcinoma. In posterior fossa ependymomas and diffuse midline glioma, CXorf67 mimics the oncogenic histone H3K27M, inhibiting PRC2 function and altering chromatin states. In endometrial stromal sarcoma, CXorf67 forms fusion genes with MBTD1, potentially disrupting polycomb group (PcG) functions. Additionally, CXorf67's interaction with PALB2 affects the BRCA1-PALB2-BRCA2 complex, influencing DNA repair mechanisms. These findings highlight CXorf67's dual role in epigenetic regulation and DNA damage response, suggesting its potential as a therapeutic target. However, further research is needed to explore its functions in other cancers and clarify its molecular mechanisms. Our review synthesizes current knowledge on CXorf67's biological significance, particularly in epigenetics and DNA damage, and its implications in oncogenesis. - Source: PubMed
Publication date: 2025/11/10
Yu XinningWu HuataoLan YangzhengChen WenjiaLiu Jing - Myeloid/NK cell precursor leukemia (MNKPL) is a rare, aggressive entity often misdiagnosed as acute myeloid leukemia (AML) or aggressive NK cell leukemia (ANKL) because of overlapping markers (CD7, CD13/CD33, CD56, myeloperoxidase [MPO]-). We report a patient initially diagnosed with ANKL; subsequent flow-cytometric reevaluation (CD7, CD13, CD33, CD34, CD56, CD117, MPO) supported a diagnosis of MNKPL. RNA sequencing and nested PCR identified an in-frame ZMYND11::MBTD1 fusion. A review of published ZMYND11::MBTD1 leukemias (n = 5) found immunophenotypes highly consistent with MNKPL, suggesting prior misclassification. These findings support ZMYND11::MBTD1 as a recurrent lesion in MNKPL and a practical aid to diagnosis and treatment selection. - Source: PubMed
Publication date: 2025/12/27
Liang HaoSu XinChen PingZhao ShengbinGao LiDu ZhizhuoCheng ShengqinMiao JieHu ShaoyanXiao Peifang - - Source: PubMed
Publication date: 2025/11/20
Wei QingPemmaraju NaveenWang Sa AHu ShiminDinardo CourtneyIssa Ghayas CBueso-Ramos Carlos EXu JieLi ShaoyingMedeiros L JeffreyTang Guilin - Mechanisms for genome stability in actively transcribed regions are essential for cellular homeostasis; however, these mechanisms are poorly understood. Herein, we identify the bromodomain and extraterminal domain (BET) family BRD3 as the genome caretaker in actively transcribed chromatin. We identify the protein network between BRD3 and chromatin remodeler TIP60. During transcription, BRD3 localizes to actively transcribed chromatin through its N-terminal bromodomains. Following DNA double-strand breaks (DSBs) at the actively transcribed chromatin, the C-terminal extraterminal (ET) domain of BRD3 recruits CHD4 via its KIKL-like motifs to replace HP1 with the TIP60 (Tat-interactive protein, 60 kDa) complex, promoting H4K16 acetylation and MBTD1 recruitment, which creates chromatin barriers to 53BP1. This process recruits BRCA1 and R-loop-processing factors to promote R-loop-mediated homologous recombination (HR) and suppress 53BP1 and mutagenic non-homologous end-joining. Our study elucidates the mechanism by which BRD3 initiates DSB-induced chromatin remodeling by CHD4 and TIP60 to promote R-loop-mediated HR on actively transcribed chromatin to maintain genome stability. - Source: PubMed
Publication date: 2025/10/22
Qian JianghaoWatanabe TomokoWatanabe ReikoKanno Shin-IchiroTakahashi AkikoKohsaka ShinjiYoshino YukiChiba NatsukoTanaka KozoKohno TakashiYasui AkiraUi Ayako - Colorectal cancer (CRC) is intricately influenced by dysregulated microRNAs (miRNAs) targeting the Wnt signaling pathway, a phenomenon pivotal in CRC initiation and progression. The exploration of miRNA-Wnt interactions holds promise for innovative therapeutic strategies in CRC treatment. - Source: PubMed
Publication date: 2025/07/01
Amerizadeh ForouzanPasdar AlirezaAbidi Pouria