Ask about this productRelated genes to: BCL2L13 Blocking Peptide
- Gene:
- BCL2L13 NIH gene
- Name:
- BCL2 like 13
- Previous symbol:
- -
- Synonyms:
- MIL1, BCL-RAMBO
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-20
- Date modifiied:
- 2016-10-05
Related products to: BCL2L13 Blocking Peptide
Related articles to: BCL2L13 Blocking Peptide
- The canine transmissible venereal tumor (CTVT) is a naturally occurring clonal cancer that offers a unique model to study tumor evolution, immune evasion, and chemoresistance. Although vincristine induces complete remission in most cases, some tumors show partial response or resistance, and the molecular drivers of this variability remain unclear. While genomic and epigenetic studies have implicated multidrug resistance and immune modulation, transcriptional mechanisms underlying therapeutic outcomes are not fully characterized. - Source: PubMed
Publication date: 2026/04/15
López-Valbuena Fabián DOsorio-Zambrano William FDebiaso Rossi André LMontoya-Flórez Luis MRocha Noeme S - Severe Omicron cases present profound lymphocytopenia, suggesting variant-specific immune injury. - Source: PubMed
Publication date: 2026/03/28
Gao ChaoChen HanbingChi YingLu XinxingLi JiahuangTang YingYu RuixuanShi NanLiu LingXie JianfengQiu HaiboChao JieLi Shufeng - The mitogen-activated protein kinase (MAPK) pathway widely regulates development and cancer. However, the subcellular localization and function of the secondary kinases in the MAPK pathway remain unclear. Here, we identified mitogen-activated protein kinase kinase 6 or 3 (MKK6/MKK3) as tumor suppressors that could significantly activate mitophagy and suppress tumor growth in lung adenocarcinoma (LUAD). Mechanistically, among MKK1-7, only MKK6/MKK3 exhibited subcellular organellar localization in mitochondria and autophagosome interaction site. The function of MKK6 in mitophagy and tumorigenicity was dependent on its kinase activity, but not through p38. MKK6 directly phosphorylated BCL2L13 at serine 426, enhancing the interaction between BCL2L13 and LC3B, which, in turn, promoted mitophagy, inhibited oxidative phosphorylation (OXPHOS), and prevented tumor growth. Our studies not only revealed that MKK6-BCL2L13 phosphorylation at the interorganellar site can affect mitochondrial quality in tumorigenicity but also might provide a potential therapeutic strategy for LUAD treatment. - Source: PubMed
Publication date: 2026/03/24
Xing GuangsuoHuang YileLiu XiwenLi LinpengLiu ZichaoWu YiZhou YanshuangDing YingzheChen BaodanXue GuanruLi ZijingHao ZhihongLiu YangFan WenhuiDing HaolinLiang ShanHe JingcaiWang JunweiZhang JianQin DajiangWang WumingLu GangChan Wai-YeeRan PixinJu HuaiqiangDong MingLiang WenhuaLiu XingguoChen Keshi - Skeletal muscle is a heterogeneous tissue consisting of fibers with distinct contractile speeds, metabolic profiles, and cellular signaling. This heterogeneity may extend to mitochondrial quality control processes such as mitophagy. Using mt-Keima mice, we found that mitophagic activity was greater in the fast-twitch, glycolytic extensor digitorum longus (EDL) compared to the slow-twitch, oxidative soleus (SOL) muscle. Live imaging of quadriceps (QUAD) muscle revealed two distinct fiber populations: those with high total mt-Keima signal but low mitophagic activity, and others with low signal but higher mitophagic activity. Additionally, we observed skeletal muscle type and regional differences in autophagic and mitophagic protein content. Further, select mitophagic proteins strongly correlated with mitochondrial proteins across different regions of the gastrocnemius, while others did not. These findings highlight the complexity of mitophagy regulation in skeletal muscle and emphasize the importance of considering muscle phenotype, including fiber type, region, and mitochondrial content when studying mitophagy.: AIFM1: apoptosis inducing factor mitochondria associated 1; ATG: autophagy related; ATG7: autophagy related 7; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; BCL2L13: BCL2 like 13; CSA: cross-sectional area; CYCS: cytochrome c, somatic; EDL: extensor digitorum longus; FUNDC1: FUN14 domain containing 1; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GAS: gastrocnemius; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MYH: myosin heavy chain; OXPHOS: oxidative phosphorylation; PINK1: PTEN induced kinase 1; PLANT: plantaris; PRKN: parkin RBR E3 ubiquitin protein ligase; QUAD: quadriceps; SLC25A4: solute carrier family 25 member 4; SOD2: superoxide dismutase 2; SOL: soleus; SQSTM1: sequestosome 1; TFAM: transcription factor A, mitochondrial; VDAC1: voltage dependent anion channel 1. - Source: PubMed
Publication date: 2026/03/02
Rahman Fasih AGraham Mackenzie QQuadrilatero Joe - Glioblastoma multiforme (GBM), the most aggressive primary brain tumor, is associated with extremely poor patient prognosis. Temozolomide (TMZ) resistance remains a major cause of treatment failure. Protein arginine methyltransferase 6 (PRMT6) plays critical roles in tumorigenesis, but its function and regulatory mechanisms in GBM TMZ resistance have not been elucidated. While the hypoxic microenvironment is a hallmark feature of GBM, its epigenetic regulatory mechanisms in drug resistance remain unclear. - Source: PubMed
Publication date: 2026/01/02
Chen ShuyangYu PengSun YongqingYan YutingZhang BoxiangLi Guangyu