RBBP9 Antibody
- Known as:
- RBBP9 Antibody
- Catalog number:
- GWB-ML930C
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- RBBP9 Antibody
Related genes to: RBBP9 Antibody
- Gene:
- RBBP9 NIH gene
- Name:
- RB binding protein 9, serine hydrolase
- Previous symbol:
- -
- Synonyms:
- Bog
- Chromosome:
- 20p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-22
- Date modifiied:
- 2016-10-05
Related products to: RBBP9 Antibody
Related articles to: RBBP9 Antibody
- Gastric cancer remains one of the most lethal malignancies worldwide, characterized by extensive molecular heterogeneity, late diagnosis, and limited therapeutic options. Identifying key regulatory genes, upstream transcription factors, and clinically meaningful prognostic markers is essential for improving patient management and accelerating targeted drug discovery. - Source: PubMed
Publication date: 2026/04/29
Akhavan RezaForoughian MahdiAmerizadeh Forouzan - Duchenne Muscular Dystrophy (DMD) is a severe genetic disorder affecting skeletal and cardiac muscles, primarily in males. While much research has focused on these systems, the role of vascular smooth muscle cells (VSMCs) remains underexplored. This study examines how dystrophin deficiency alters VSMCs plasticity using mdx mice and DMD patient-derived iPSC VSMCs. Immunohistochemistry, Western blot, electron microscopy, and transcriptomic analyses revealed significant abnormalities. In mdx mice, abnormal vascular structure and vascular degeneration were observed. DMD VSMCs showed impaired maturation, reduced contractile protein expression, and disrupted mitochondrial dynamics, including excessive fission and reduced mitochondrial area. These cells also exhibited increased apoptosis under oxidative stress. Transcriptomic profiling identified dysregulated genes related to VSMC proliferation, differentiation, and vascular development, with transcription factors such as GADD45A, SOX9, TIA1, RBBP9, and FOXM1 implicated. Under stress, apoptotic pathways were notably upregulated. These findings suggest that dystrophin deficiency drives VSMC phenotype switching and mitochondrial dysfunction, contributing to vascular pathology in DMD. These findings highlight the importance of targeting vascular abnormalities in therapeutic strategies to slow disease progression. - Source: PubMed
Publication date: 2025/11/24
Xuan WanlingCheng FengHan XiaoweiTipparaju Srinivas MAshraf Muhammad - Retinoblastoma-binding protein 9 (RBBP9) was initially reported as cell cycle regulator via RB/E2F. Accumulating evidence has revealed the importance of RBBP9 in physiological and pathological states including inflammatory disease. However, the functional role of RBBP9 in ulcerative colitis (UC) and colitis-associated cancer (CAC) remains elusive. - Source: PubMed
Publication date: 2024/12/02
Hamada KensukeNakanishi YukiMuta YuOmatsu MayukiIwane KosukeIkeda MunehiroChen JiayuMasui YokoAoyama NaokiAgatsuma NobukazuYamakawa GoUtsumi TakahiroKitamoto HirokiOkabe MakotoItatani YoshiroAdachi TakumiYasuda KoubunYamamoto ShujiFukuda AkihisaKuroda EtsushiOhmuraya MasakiObama KazutakaHirota SeiichiIkeuchi HirokiNakanishi KenjiSeno Hiroshi - Fanconi anaemia (FA) is a rare chromosomal-instability syndrome caused by mutations of any of the 22 known FA DNA-repair genes. FA individuals have an increased risk of head-and-neck squamous-cell-carcinomas (HNSCC), often fatal. Systemic intolerance to standard cisplatin-based protocols due to somatic-cell hypersensitivity underscores the urgent need to develop novel therapies. Here, we performed unbiased siRNA screens to unveil genetic interactions synthetic-lethal with FA-pathway deficiency in FA-patient HNSCC cell lines. We identified based on differential-lethality scores between FA-deficient and FA-proficient cells, next to common-essential genes such as PSMC1, PSMB2, and LAMTOR2, the otherwise non-essential RBBP9 gene. Accordingly, low dose of the FDA-approved RBBP9-targeting drug Emetine kills FA-HNSCC. Importantly both RBBP9-silencing as well as Emetine spared non-tumour FA cells. This study provides a minable genome-wide analyses of vulnerabilities to address treatment challenges in FA-HNSCC. Our investigation divulges a DNA-cross-link-repair independent lead, RBBP9, for targeted treatment of FA-HNSCCs without systemic toxicity. - Source: PubMed
Publication date: 2023/01/13
Pai GovindRoohollahi KhashayarRockx Davyde Jong YvonneStoepker ChantalPennings CharlotteRooimans MartinVriend LiannePiersma SanderJimenez Connie RDe Menezes Renee XVan Beusechem Victor WBrakenhoff Ruud HTe Riele HeinWolthuis Rob M FDorsman Josephine C - We previously observed the beneficial role of folic acid supplemented from maternal or offspring diet on lamb growth performance and immunity. Twenty-four Hu lambs from four groups (mother received folic acid or not, offspring received folic acid or not) were used in the current study, which was conducted consecutively to elucidate the molecular regulatory mechanisms of folic acid in lambs by analyzing blood metabolome, liver transcriptome, and muscle transcriptome. Serum metabolomics analysis showed that L-homocitrulline, hyodeoxycholic acid, 9-Hpode, palmitaldehyde, N-oleoyl glycine, hexadecanedioic acid, xylose, 1,7-dimethylxanthine, nicotinamide, acetyl-N-formyl-5-methoxykynurenamine, N6-succinyl adenosine, 11-cis-retinol, 18-hydroxycorticosterone, and 2-acetylfuran were down-regulated and methylisobutyrate was up-regulated by the feeding of folic acid from maternal and/or offspring diets. Meanwhile, folic acid increased the abundances of and but decreased in the liver. In the muscle, , and were up-regulated, and were down-regulated by the feeding of folic acid. The pathways of bile secretion, biosynthesis of unsaturated fatty acids, linoleic acid metabolism, and herpes simplex virus 1 infection were changed by folic acid in blood, liver, or muscle. Further integrated analysis revealed potential interactions among the liver, blood, and muscle, and the circulating metabolites, hub gene, and pathways, which might be the predominant acting targets of folic acid in animals. These findings provide fundamental information on the beneficial function of folic acid no matter from maternal or offspring, in regulating animal lipid metabolism and immune enhancement, providing a theoretical basis for the use of folic acid from the view of animal health care. - Source: PubMed
Publication date: 2022/08/12
Wang BingLi HeqiongLi ZhenWang BoZhang HanZhang BoyanLuo Hailing