Acetone Oxime Tech
- Known as:
- Acetone Oxime Tech
- Catalog number:
- A04590
- Product Quantity:
- 100 G
- Category:
- -
- Supplier:
- pfalslandbauer.
- Gene target:
- Acetone Oxime Tech
Related genes to: Acetone Oxime Tech
- Gene:
- PLEKHG5 NIH gene
- Name:
- pleckstrin homology and RhoGEF domain containing G5
- Previous symbol:
- -
- Synonyms:
- KIAA0720, Syx, GEF720, Tech
- Chromosome:
- 1p36.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-23
- Date modifiied:
- 2019-04-23
Related products to: Acetone Oxime Tech
Related articles to: Acetone Oxime Tech
- Thyroid eye disease (TED) is a debilitating condition characterized by orbital fibroblast (OF) activation and excessive hyaluronan (HA) accumulation within the retroocular space. While IGF-1R blockade has significantly advanced TED management, incomplete clinical responses and disease relapse underscore the need to identify alternative targets. - Source: PubMed
Publication date: 2026/08/19
Yuan KyleTruong PhillipPatrick Charkira CUshchak EmmaRoztocil ElisaFeldon Steven EWoeller Collynn F - Biallelic pathogenic variants in PLEKHG5 are associated with two distinct recessive phenotypes, including distal hereditary motor neuropathy AR type 4 and intermediate Charcot-Marie-Tooth disease type C (CMT). No South American cases have been previously reported. - Source: PubMed
Vidon Rafael OliveiraTomaselli Pedro JoséBittar-Braune CarolinePitta Izabela Jardimde Lacerda Glenda Corrêa BorgesJardim Márcia - Atg9-containing vesicles are enriched in synapses and undergo cycles of exo- and endocytosis similarly to synaptic vesicles, thereby linking presynaptic autophagy to neuronal activity. Dysfunction of presynaptic autophagy is a pathophysiological mechanism in motoneuron disease (MND), which leads to impaired synaptic integrity and function. Here, we asked whether boosting neuronal activity by physical exercise modulates the cellular and motor phenotypes of Plekhg5-deficient mice, an MND model with defective presynaptic autophagy. - Source: PubMed
Publication date: 2025/12/16
Veh AlexanderEwald Melissada Cruz Neris Geßner ViniciusGiridhar Neha JadhavHutchings Amy-JayneStigloher ChristianBinotti BeyenechHeinze Katrin GertrudLüningschrör Patrick - Endometriosis (EMS) is a chronic gynecological disease. RND3 is recognized as a potential autophagy-related biomarker in EMS. The aim of this study was to investigate the regulatory role of RND3 on autophagy and oxidative stress in EMS. Immunohistochemistry (IHC), RT-qPCR, and western blot (WB) analyses were used to determine the expression levels of RND3 and PLEKHG5. The study assessed oxidative stress by examining NRF2/NQO-1/HO-1 expression, as well as GSH, SOD, MDA levels, and lipid ROS production. Autophagy was evaluated by analyzing the expression of autophagy-related markers and phosphorylation of PI3K, AKT, ERK1/2, and mTOR. Cell proliferation, migration, and invasion were evaluated using CCK-8 and Transwell assays. Apoptosis was assessed through flow cytometry, expression of apoptosis-related markers, and TUNEL assay. The study also used ELISA to measure inflammatory factor levels and Co-IP assay to investigate the interaction between RND3 and PLEKHG5. Low expression of RND3 was observed in both the eutopic and ectopic endometrial tissues and ectopic endometrial stromal cells (EESCs) from patients with EMS. Increasing RND3 levels reduced oxidative stress in EESCs, enhanced cellular autophagy, inhibited cell proliferation, migration, and invasion, and promoted apoptosis. Conversely, the knockdown of RND3 expression had the opposite effect. The impact of RND3 overexpression on oxidative stress, autophagy, and apoptosis in EESCs was reversed by si-NRF2 and the autophagy inhibitor CQ. RND3 overexpression also upregulated the expression of PLEKHG5 in EESCs. Co-IP results revealed an interaction between RND3 and PLEKHG5. In in vivo experiments, low PLEKHG5 expression was observed in endometrial tissues of EMS mice, while RND3 overexpression alleviated EMS symptoms by decreasing oxidative stress and promoting cellular autophagy and apoptosis. RND3 inhibits EMS progression by enhancing autophagy and suppressing oxidative stress through PLEKHG5. - Source: PubMed
Li HanChai Xiaoshan - Mechanisms by which prior tuberculosis (TB) increases long-term risk for cancer, cardiovascular, and neurological disorders remain unclear, particularly in people with HIV (PWH). This study investigated DNA methylation (DNAm) patterns and associated pathways in PWH with and without prior TB infection. DNAm was analyzed in blood samples from 30 PWH (10 with prior latent TB infection [LTBI], 10 with previous successfully treated active TB, and 10 with no TB) using the Illumina MethylationEPIC BeadChip covering over 850,000 CpG sites. Epigenetic age was estimated, and age acceleration was calculated. Differentially methylated CpGs (dmCpGs) and regions (DMRs) were identified, and functional enrichment analyses for Gene Ontology, KEGG pathways, PANTHER database, and gene set enrichment analysis (DisGeNET, dbGaP) were performed. Statistical significance was set at a false discovery rate (FDR) of < 0.05. PWH exhibited significant epigenetic age acceleration, with a mean of 19.32 ± 10.82 years greater than chronological age. This accelerated aging was more pronounced in individuals with any prior TB infection (21.60 ± 12.03 years) compared to those without TB (17.42 ± 9.38 years). In the prior active TB vs. no TB comparison, 7461 dmCpGs were identified, corresponding to 150 DMRs (p < 0.05), with top associated genes including GRAMD1C (hypomethylation), DPP6 (hypermethylation), and HDAC4 (hypomethylation). In the LTBI vs. no TB comparison, 8598 dmCpGs were observed, corresponding to 39 DMRs (p < 0.05), associated with genes such as PLEKHG5 (hypermethylation), STK32C (hypermethylation), and SPATC1L. When comparing any prior TB (active or latent) to no TB, 71,774 dmCpGs and 14 DMRs were identified, including genes like PLEKHG5, KCNN3, and BRSK2. Pathway analyses of prior TB (active or latent) vs. no TB revealed enrichment in neurogenesis, neuron differentiation, axon guidance, and neuroactive ligand signaling. Additional enriched pathways included those related to platelet activation, vascular muscle contraction, and chemokine signaling. Cancer-related pathways such as proteoglycans in cancer, small cell lung cancer, prostate cancer, breast cancer, hepatocellular carcinoma, and thyroid cancer were also enriched. PANTHER analysis showed consistent enrichment in the Wnt signaling pathway and inflammation-mediated pathways across compared groups. DisGeNET analysis linked prior TB DNAm patterns to lymphoid leukemia, while dbGaP analysis identified associations with phenotypes like asthma, body mass index, tunica media, and lymphocyte count. Prior TB infection in PWH is associated with distinct DNAm changes in pathways related to neural function, cardiovascular health, and cancer risk, and is linked to more pronounced epigenetic age acceleration, suggesting epigenetic mechanisms for TB-related long-term complications. - Source: PubMed
Publication date: 2025/08/19
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