Ask about this productRelated genes to: PHB2 antibody
- Gene:
- PHB2 NIH gene
- Name:
- prohibitin 2
- Previous symbol:
- -
- Synonyms:
- REA, BCAP37, Bap37, p22
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-24
- Date modifiied:
- 2016-10-05
Related products to: PHB2 antibody
Related articles to: PHB2 antibody
- To investigate the regulatory role of the protein encoded by circUSP25 in proliferation and migration of colon cancer cells. - Source: PubMed
Li XiaominXu JieGao CaiyueZhu JijunWang YuLi DongdongWang Xiaoyan - Obesity impairs male reproductive function via oxidative stress and mitochondrial dysfunction. Kisspeptin-10 may regulate redox balance and mitochondrial homeostasis, but its role in obesity-related testicular dysfunction remains unclear. This study aimed to investigate whether Kisspeptin-10 ameliorates obesity-induced testicular oxidative stress and sperm dysfunction, with particular emphasis on mitophagy, autophagy, and apoptosis-related pathways. Forty male Sprague Dawley rats were divided into four groups: Control, Obesity, Kisspeptin-10, and Obesity+Kisspeptin-10. Obesity was induced by feeding rats a high-fat diet (60% kcal from fat) for 12 weeks. At the end of week 12, rats with a Lee index ≥ 300 were considered obese. During the subsequent 4-week treatment period, the Obesity and Obesity+Kisspeptin-10 groups continued to receive the high-fat diet, whereas the Control and Kisspeptin-10 groups continued to receive the standard diet. Kisspeptin-10 (50 nmol/kg, i.p.) was administered to both the Kisspeptin-10 and Obesity+Kisspeptin-10 groups from week 13 to week 16. Oxidative stress markers in the testes, sperm parameters, sperm mitochondrial membrane potential (MMP), and sperm deoxyribonucleic acid (DNA) integrity were assessed; in addition, protein expression levels of markers for mitophagy, autophagy, and apoptosis were evaluated. Obesity impaired antioxidant capacity, sperm quality, mitochondrial function, and reproductive organ weight, while increasing lipid peroxidation and sperm abnormalities. Kisspeptin-10 reduced oxidative stress by lowering malondialdehyde (MDA) and increasing glutathione (GSH) levels, improved sperm motility and concentration, reduced tail abnormal sperm ratio, showed a non-significant tendency toward partial restoration of mitochondrial function, decreased DNA damage, and increased prostate weight. It was also associated with increased expression of the mitophagy-related proteins PTEN-induced putative kinase 1 (PINK1) and Prohibitin 2 (PHB2), and increased Beclin-1 expression, with no significant effects on Parkin, Microtubule-associated protein 1 light chain 3-II (LC3-II), or apoptosis-related proteins. Kisspeptin-10 may alleviate obesity-induced testicular dysfunction, potentially through modulation of redox balance and mitochondrial quality-control mechanisms, including changes in mitophagy- and autophagy-related protein expression. Although these findings suggest that Kisspeptin-10 is a promising candidate for the treatment of obesity-related male infertility, its effects on downstream autophagy-related signaling and apoptosis appear to be limited. - Source: PubMed
Publication date: 2026/09/28
Arkalı GözdeÇay MehmetGüler Ekmen EdanurAcısu Tutku CanFi̇ri̇k MustafaToz AbdullahYüce AbdurraufAksakal Mesut - Parkinson's disease (PD) is a prevalent age-related neurodegenerative disorder characterized by pathological α-synuclein aggregation, mitochondrial dysfunction, and progressive loss of dopaminergic neurons, with no effective disease-modifying treatment available. Sephin1 has been proven to exert protective effects in multiple models of proteostasis diseases. However, its therapeutic potential and the underlying mechanisms in PD remain largely uncharacterized. To investigate the neuroprotective effects and mechanisms of Sephin1 in PD models, we used α-synuclein pre-formed fibrils (PFFs)-stimulated SH-SY5Y cells and primary midbrain neurons for in vitro assays, and A53T transgenic mice for in vivo evaluation. Neurotoxicity, mitochondrial function, mitophagy flux, and α-synuclein pathology were assessed. Limited proteolysis mass spectrometry (Lip-MS), surface plasmon resonance (SPR) assays, cellular thermal shift assay (CETSA), and molecular docking were applied to identify and validate direct targets. In vitro experiments revealed that Sephin1 alleviated PFFs-induced α-synuclein neurotoxicity in a dose-dependent manner. It restored mitochondrial homeostasis and inhibited oxidative stress through PINK1-PRKN-mediated mitophagy, independent of the canonical GADD34 pathway. Mechanistically, Sephin1 directly bound Prohibitin-2 (PHB2), strengthened the PHB2-LC3B interaction, and activated the PARL-PGAM5-PINK1 signaling axis. In vivo, Sephin1 mitigated motor dysfunction, rescued defective mitophagy, and attenuated α-synuclein pathology in A53T mice. Collectively, our findings establish the protective effect of Sephin1 in PD and uncover a previously unrecognized mechanism by which Sephin1 directly targets PHB2 to activate mitophagy. - Source: PubMed
Publication date: 2026/09/25
Ding Xv-ShenWang BaoHan ZhengCao JieLi Yang-NiFeng Chen-XiWang Yu-FeiGuru Jian-CaiWang Xue-LianYang QianQu YanGao Li - Certain dairy products have been reported to reduce the risk of cognitive decline in older adults and patients with Alzheimer's disease (AD). Intake of the whey-derived tetrapeptide Gly-Thr-Trp-Tyr (GTWY) improves mild cognitive impairment in healthy adults, while GTWY administration in mice suppresses AD-like pathologies, including amyloid-beta (Aβ) accumulation and neuroinflammation. GTWY treatment also reduces Aβ-induced mitochondrial dysfunction in neuronal cells. However, the molecular mechanisms underlying these effects remain unclear. Here, we identified prohibitin 2 (PHB2) as a direct binding partner of GTWY in human neuroblastoma SH-SY5Y cells and investigated its role in the mitochondrial protective effect of GTWY. GTWY treatment increased the abundance of the prohibitin complex detected by blue native PAGE without affecting PHB1 or PHB2 expression. Moreover, PHB2 knockdown abolished the mitochondrial protective effect of GTWY, indicating that PHB2 mediates this effect. These findings suggest that GTWY binding to PHB2 modulates the functional state of the prohibitin complex, thereby preserving mitochondrial function. Our results provide new insights into the molecular mechanisms underlying the mitochondrial protective effects of whey-derived peptides and highlight the potential role of the prohibitin complex in mediating these effects. - Source: PubMed
Publication date: 2026/09/21
Mizukami NoaMiwa KotohaUmeda KentaroFukuda TakafumiTakano NaoharuHiramoto Masaki - Induced pluripotent stem cell-derived immortalized megakaryocyte cell lines (imMKCLs) exhibit substantial heterogeneity, which poses a major barrier to efficient ex vivo production of platelet-like particles (PLPs). In this study, we combined proteomic profiling with principal component analysis to uncover regulatory factors influencing imMKCL maturation. Through correlation-based omics screening, prohibitin 2 (PHB2) was identified as a putative inhibitory node, and JI051, a small molecule previously reported to bind PHB2, was found to enhance PLP production. JI051 accelerated proplatelet-like extensions and increased PLP yield without affecting basic functional markers. Transcriptomic analysis showed that JI051 induced transcriptional changes consistent with megakaryocyte maturation and PLP biogenesis. Together, these findings identify JI051 as an enhancer of platelet biogenesis and provide a strategy to mitigate cellular heterogeneity in imMKCL megakaryocytes for scalable artificial platelet production, with potential benefits for emergency blood supply and cost-effective bioproduction. - Source: PubMed
Publication date: 2026/09/23
Taga RyosukeKuwano NozomiHarada YasuoHayashi TakashiSakamoto YukiFujio KosukeKakumoto YusukeNakamura EmiriEto KojiHayashi Hideki