CENTD3 _ ARAP3
- Known as:
- CENTD3 _ ARAP3
- Catalog number:
- Y213274
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CENTD3 _ ARAP3
Related genes to: CENTD3 _ ARAP3
- Gene:
- ARAP3 NIH gene
- Name:
- ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 3
- Previous symbol:
- CENTD3
- Synonyms:
- FLJ21065, DRAG1
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-10
- Date modifiied:
- 2015-09-11
Related products to: CENTD3 _ ARAP3
Related articles to: CENTD3 _ ARAP3
- This study established an optimized process for obtaining anti-aging peptides from mushroom feet (PEMFPeps). Using response surface methodology, high yields of protein (51.31 ± 3.00%) and peptides (48.71 ± 0.17% hydrolysis degree) were achieved. In a D-galactose-induced PC12 cell aging model, the simulated digests (SID-PEMFPeps) exhibited potent anti-aging effects at a concentration of 1 mg/mL. An integrated transcriptomic and metabolomic approach was employed to systematically investigate the underlying mechanisms. The results revealed that Integrated transcriptomic and metabolomic analyses showed that SID-PEMFPeps alleviated cellular senescence through multi-dimensional regulation of transcriptional and metabolic networks. This included modulating key pathways related to oxidative stress, synaptic function, and energy metabolism (e.g., glutamatergic synapse, pentose phosphate pathway, and TCA cycle), and reversing the aberrant expression of aging-associated genes (e.g., ). Our findings demonstrate that SID-PEMFPeps are promising candidates for functional foods targeting age-related dysfunction though their efficacy and safety in vivo require further validation. - Source: PubMed
Publication date: 2025/11/20
Wang ShangmengLi HaiyanZhao FenGao Ji'anHuang ShuaishuaiLiu XinqiMa Biao - Moyamoya disease (MMD) is a chronic, progressive occlusive cerebrovascular disease. It causes recurrent cerebrovascular stroke due to vascular closure and proliferation. An unclear pathophysiological mechanism is the most significant obstacle in the diagnosis and treatment of MMD. - Source: PubMed
Publication date: 2025/07/28
Zhou ZhenyuNiu HongchuanXu ShaoqiZhang JunzeLiu YutongLei ChengxuHe ShihaoZhao Yuanli - Chronic kidney disease (CKD), characterized by gradual loss of renal function, may be driven by environmental exposure such as perfluoroalkyl and polyfluoroalkyl substances (PFAS), yet the intrinsic mechanisms are largely unknown. Here, we observed distinct proteinuria in the mice exposed to sodium -perfluorous nonenoxybenzenesulfonate (OBS), an alternative to perfluorooctanesulfonate. The renal S-adenosylhomocysteine (SAH) level increased due to the decrease in its hydrolase adenosylhomocysteinase (AHCY), and was positively correlated with the observed proteinuria. Consequently, the DNA methylation level was downregulated. Specifically, the promoter methylation of increased, while the genebody methylation of decreased, thereby causing downregulation of their mRNA expressions. This further suppressed the levels of Rho GTPases and , which then reduced their downstream genes , and , and eventually inhibited expression. Consequently, the podocyte cytoskeleton was disrupted, promoting foot process fusion and inducing proteinuria. Overexpression of AHCY in OBS-exposed mice reduced the level of SAH, restored the methylation levels and gene expressions, ameliorated the podocyte injury, and eventually reduced the level of urinary protein. Taken together, inhibition of AHCY was the molecular initiating event of OBS-induced proteinuria, which functioned through the AHCY-SAH-Arap3/Tiam1-RhoA/Rac1-Pip5k1a/Pip5k1b/Pip5k1c-Actn4 axis. This study provides profound insight into the potential risk of PFAS in disrupting renal function and kidney health. - Source: PubMed
Publication date: 2025/05/30
Lyu YangGuo RuyuZhong WenjueZhu Lingyan - SEPT9 is a pivotal cytoskeletal GTPase that regulates diverse biological processes encompassing mitosis and cytokinesis. While previous studies have implicated SEPT9 in tumorigenesis and development; comprehensive pan-cancer analyses have not been performed. This study aims to systematically explore its role in cancer screening, prognosis, and treatment, addressing this critical gap. - Source: PubMed
Publication date: 2024/09/05
Wang WenwenZhang XiaochenGui PingZou QizhenNie YuzhouMa ShenglinZhang Shirong - Vascular permeability is temporarily heightened during inflammation, but excessive inflammation-associated microvascular leakage can be detrimental, as evidenced in the inflamed lung. Formylated peptides regulate vascular leakage indirectly via formylated peptide receptor-1 (FPR1)-mediated recruitment and activation of neutrophils. Here we identify how the GTPase-activating protein ARAP3 protects against formylated peptide-induced microvascular permeability via endothelial cells and neutrophils. In vitro, Arap3 endothelial monolayers were characterised by enhanced formylated peptide-induced permeability due to upregulated endothelial FPR1 and enhanced vascular endothelial cadherin internalisation. In vivo, enhanced inflammation-associated microvascular leakage was observed in Arap3 mice. Leakage of plasma protein into the lungs of Arap3 mice increased within hours of formylated peptide administration. Adoptive transfer experiments indicated this was dependent upon ARAP3 deficiency in both immune and non-immune cells. Bronchoalveolar lavages of formylated peptide-challenged Arap3 mice contained neutrophil extracellular traps (NETs). Pharmacological inhibition of NET formation abrogated excessive microvascular leakage, indicating a critical function of NETs in this context. The observation that Arap3 mice developed more severe influenza suggests these findings are pertinent to pathological situations characterised by abundant formylated peptides. © 2024 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2024/05/11
Chu Julia YMcCormick BarrySundaram KruthikaHardisty GarethKarmakar UtsaPumpe CarolineKrull ElizabethLucas Christopher DAmado-Azevedo JoanaHordijk Peter LCaporali AndreaMellor HarryBaillie J KennethRossi Adriano GVermeren Sonja