Ambra1 Rabbit Polyclonal Antibody
- Known as:
- Ambra1 Rabbit Polyclonal Antibody
- Catalog number:
- AUT-4557
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- Ambra1 Rabbit Polyclonal Antibody
Ask about this productRelated genes to: Ambra1 Rabbit Polyclonal Antibody
- Gene:
- AMBRA1 NIH gene
- Name:
- autophagy and beclin 1 regulator 1
- Previous symbol:
- -
- Synonyms:
- FLJ20294, KIAA1736, WDR94, DCAF3
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-02-01
- Date modifiied:
- 2016-04-28
Related products to: Ambra1 Rabbit Polyclonal Antibody
Related articles to: Ambra1 Rabbit Polyclonal Antibody
- Glioblastoma harbors frequent alterations in the retinoblastoma (RB1) pathway, providing a genetic rationale for therapeutic targeting with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors. The NOA-20 trial did not reveal a progression-free survival benefit of CDK4/6 inhibition plus radiation therapy in newly diagnosed, MGMT-unmethylated glioblastoma. In fact, CDK4/6 inhibitor monotherapy has not demonstrated efficacy in solid tumors. We aimed at discovering response modulators to CDK4/6 inhibition, paving the way for rational combination therapies. - Source: PubMed
Publication date: 2026/05/04
Surender SurenderHaeusser Lara AnninaKuhlburger LaurenceTsiami FoteiniDogan Nihal OlcayMaise LouiseNahnsen SvenBeck SusanneMerk Daniel JosefTabatabai Ghazaleh - Neural progenitor cell (NPC) proliferation is fundamental for population expansion and brain development. G phase control determines the cell cycle duration of NPCs and thereby affects their proliferation efficiency. However, the molecular mechanisms governing G phase progression in NPCs remain unclear. Here, we show that AKT gain-of-function mutations and pharmacological inhibition exert opposing effects on NPC proliferation. Consistently, Emx1-Cre-mediated deletion of Akt1/2/3 in mice impairs NPC proliferation and disrupts cortical development. We find that AKT deficiency induces G phase arrest and prolongs the cell cycle of NPCs. Mechanistically, we demonstrate that AKT-mediated phosphorylation inhibits the activity of CRL4 E3 ubiquitin ligase to safeguard cyclin D2 (CCND2) stability. Specifically, AKT phosphorylates DDB1, the adaptor of CRL4, which disrupts its interaction with CCND2 and reduces its degradation. These findings reveal a post-translational mechanism impacting NPC cell cycle and cortical morphogenesis, providing insight into the etiology of malformations of cortical development. - Source: PubMed
Publication date: 2026/04/27
Wang HeLiu PanmiaoWang RunminGu HanwenZhu TingtingChen GuiquanYang Jian-Jun - AMBRA1 (autophagy and beclin 1 regulator 1) is primarily recognized as a tumor suppressor. However, its role as a tumor promoter has garnered increasing attention. Here, leveraging clinical data of an international multi-omic medulloblastoma (MB) cohort, we identified that elevated AMBRA1 protein levels, independently of its mRNA expression, correlate with poor prognosis in the Sonic Hedgehog subgroup (MB). Mechanistically, AMBRA1 enhances SHH signaling by stabilizing GLI1, the pathway's final effector, via inhibition of its βTrCP-mediated degradation. Additionally, AMBRA1 protein stability is modulated by the REN E3 ubiquitin ligase, a tumor suppressor gene lost in MB. Inhibition of AMBRA1 blocks MB growth in murine and patient-derived preclinical models. Moreover, combining AMBRA1 knockdown with FDA-approved SHH inhibitors enhances antitumor efficacy. These findings identify the AMBRA1/βTrCP/REN axis as a key regulatory mechanism in SHH signaling and discover an unrecognized function of AMBRA1 in MB, providing actionable insights into brain tumor biology. - Source: PubMed
Publication date: 2026/04/13
Basili IreneBufalieri FrancescaConenna MarilisaNavacci ShirinLi Yue-RuTorrejon JacobBernardi FlaviaLospinoso Severini LudovicaMarsaud VeroniqueCancila GabrieleBourmeau GuillaumeYu HuaLo Re ValentinaTalbot JulieAdabbo GennaroDi Pinto AlbericoAgnoli FrancescaGiovannini DanielaLeonardi SimonaBordone RosaPetroni MarialauraSouphron JudithBlauwblomme ThomasBeccaria KévinDufour ChristelleD'Angelo LucaDe Smaele EnricoCanettieri GianlucaGiannini GiuseppeFimia Gian MariaMaroder MarellaGuardavaccaro DanielePazzaglia SimonettaTsai Jin-WuInfante PaolaAyrault OlivierDi Marcotullio Lucia - Mycotoxin contamination poses a major challenge to public health and has garnered increasing attention across the world in recent decades. Zearalenone (ZEA), as one of the most prevalent contaminants, induces reproductive toxicity and then poses potential threats to animal health. Autophagy/beclin-1 regulator 1 (AMBRA1) is a protein critical for autophagy induction, and can enhance mitophagy by co-localizing with LC3. However, the potential health risk caused by ZEA in male germ cells of animals is unclear. This study aimed to investigate the underlying mechanisms of ZEA-induced swine testicular (ST) cell injury and to clarify the role of AMBRA1 in this process. - Source: PubMed
Publication date: 2026/03/14
Hu ZiyanYang ShangjiaZhang XiaoyiLou MingYu QiCheng YueChang YuanhuangJiang FuweiChen MingshanWang JiaxinSong YijiaZheng JingMao XinyueWang YiboLi JinlongZhao Yi - Prothrombin gene mutations can be associated with either a thrombotic or a bleeding risk. Genomic studies and coagulation workup can provide valuable information to better understand their clinical importance. - Source: PubMed
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