ANAPC13
- Known as:
- ANAPC13
- Catalog number:
- 001559A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANAPC13
Related genes to: ANAPC13
- Gene:
- ANAPC13 NIH gene
- Name:
- anaphase promoting complex subunit 13
- Previous symbol:
- -
- Synonyms:
- SWM1, APC13, DKFZP566D193
- Chromosome:
- 3q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-24
- Date modifiied:
- 2016-10-04
Related products to: ANAPC13
Related articles to: ANAPC13
- Oocyte maturation arrest is an intractable clinical problem, resulting in recurrent failure of assisted reproductive treatments. The anaphase-promoting complex or cyclosome orchestrates a series of proteolytic events to ensure proper cell cycle progression of mitosis in somatic cell proliferation and meiosis during oocyte maturation. Defects in anaphase-promoting complex or cyclosome subunits, such as ANAPC8 and ANAPC12, have been demonstrated linked to oocyte maturation arrest. However, the roles of other anaphase-promoting complex or cyclosome subunits in oocyte maturation remain unclear. - Source: PubMed
Publication date: 2026/04/15
Wang YuDing ZhimingLiu XuemeiLiu XuTan HujiaZheng NaYu KexinChen BiaobangWang FengsongCao YunxiaHuang LingliSang QingZhu Fuxi - Hepatocellular carcinoma (HCC) poses a considerable global health challenge, notably due to the resistance to sorafenib therapy, which significantly impedes effective treatment strategies. This study aimed to identify potential resistance-associated genes and develop a robust prognostic model to predict patient outcomes. - Source: PubMed
Publication date: 2025/08/20
He KuanHui HongyanZhou FangLiu KaiZhao XiLiu Jun - Breast cancer is a heterogeneous disease with diverse molecular subtypes, underscoring a better understanding of its molecular features and underlying regulatory mechanisms. Therefore, identifying novel prognostic biomarkers and therapeutic targets is crucial for advancing the current standard of care for breast cancer patients. - Source: PubMed
Publication date: 2024/11/13
Abohalawa Bushra YasinShaath HibahElango RameshVishnubalaji RadhakrishnanRashid SameeraAl-Sarraf ReemAkhtar MohammedAlajez Nehad M - Recurrent somatic mutations in spliceosome factor 3b subunit 1 (SF3B1) are identified in hematopoietic malignancies, with SF3B1-K700E being the most common one. Here, we show that regulatory T cell (T)-specific expression of SF3B1-K700E () results in spontaneous autoimmune phenotypes. CD4 T cells from mice display defective T differentiation and inhibitory function, which is demonstrated by failed prevention of adoptive transfer colitis by T. Mechanically, SF3B1-K700E induces an aberrant splicing event that results in reduced expression of a cell proliferation regulator due to the insertion of a 231-base pair DNA fragment to the 5' untranslated region. Forced expression of the gene restores the differentiation and ability of T to prevent adoptive transfer colitis. In addition, acute myeloid leukemia grows faster in aged, but not young, mice compared to mice. Our results highlight the impact of cancer-associated mutation on immune responses, which affect cancer development. - Source: PubMed
Publication date: 2024/09/20
Shi YunZhang WencanJia QiongZhong XiancaiIyer PrajishWu HongminYuan Yate-ChingZhao YuqiZhang LianjunWang LiliJia ZhenyuKuo Ya-HueiSun Zuoming - Somatic mutations in coding regions of the genome may result in non-functional proteins that can lead to cancer or other diseases, however cancer mutations in the non-coding regions have rarely been studied and the interpretation of their effects is difficult. Non-coding mutations might act by breaking or creating transcription factor binding motifs in promoters, enhancers or silencers resulting in altered expression of target gene(s). A high number of mutations have been reported in coding and non-coding regions in cells of liver cancer. Hepatocyte nuclear factor 4α is a transcription factor that regulates the expression of several genes in liver cells, while the motifs it binds are frequently mutated in promoters and enhancers in liver cancer. - Source: PubMed
Cavalli MDiamanti KPan GDabrowski M JKomorowski JWadelius C