Ask about this productRelated genes to: SSBP1 Blocking Peptide
- Gene:
- SSBP1 NIH gene
- Name:
- single stranded DNA binding protein 1
- Previous symbol:
- -
- Synonyms:
- SSBP, mtSSB
- Chromosome:
- 7q34
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-29
- Date modifiied:
- 2016-03-18
Related products to: SSBP1 Blocking Peptide
Related articles to: SSBP1 Blocking Peptide
- The global decline in male fertility highlights the need to understand the mechanisms of spermatogenesis. Mitochondrial dysfunction and ferroptosis have emerged as key contributors to spermatogenic impairment, although the molecular basis of this process is still poorly defined. F-Box Protein 39 (FBXO39), a testis-enriched F-box protein, has been preliminarily associated with cell survival. However, whether FBXO39 participates in mitochondrial functional regulation or ferroptosis signaling during spermatogenesis remains largely unexplored. In our study, FBXO39 knockdown resulted in abnormal testicular development, impaired spermatogenesis, abnormal sperm morphology, and reduced testicular cell viability. Further analysis revealed that FBXO39 deficiency caused mitochondrial dysfunction and ferroptosis, as reflected by decreased ATP production, reduced mitochondrial DNA content, elevated eactive oxygen species (ROS) levels, diminished expression of key mitochondrial proteins, and elevated lipid peroxidation. Mechanistically, FBXO39 maintains mitochondrial homeostasis by targeting lysine-specific demethylase 5A (KDM5A) for ubiquitination-dependent degradation. Conversely, the accumulation of KDM5A upon FBXO39 loss suppressed single-stranded DNA-binding protein 1 (SSBP1) levels through demethylation of Histone H3 lysine 4 trimethylation (H3K4me3) at the SSBP1 promoter. Importantly, restoration of SSBP1 expression functionally ameliorated mitochondrial dysfunction induced by FBXO39 knockdown. Overall, FBXO39 regulates mitochondrial function and ferroptosis in testicular cells through ubiquitinating KDM5A, which affects SSBP1 expression by modulating H3K4me3 demethylation at the SSBP1 promoter. This study elucidates the role of FBXO39 in spermatogenesis and suggested that targeting this regulatory axis may offer novel therapeutic strategies for male infertility. - Source: PubMed
Publication date: 2026/03/04
Li TaoWang KunChen YuxiangLi ZhuochengLi ShandaZhang YuZhu XuyuanShi HaoranGao LiangJiang Hongtao - - Source: PubMed
Jiang Hong-LinSun He-FenGao Shui-PingLi Liang-DongHuang ShengHu XinLiu ShengWu JiongShao Zhi-MingJin Wei - Exome sequencing solved 26% of nephronophthisis cases, identifying nephropathy and extrarenal disease genes beyond classic ciliopathy panels. Exome sequencing uncovered GN and tubular nephropathy genes misdiagnosed as ciliopathy-associated nephropathy, underscoring diagnostic overlap in kidney diseases. Patients with nonciliary genetic variants may present with ciliopathy-like extrarenal symptoms, showing phenocopies in kidney ciliopathy diagnostics. - Source: PubMed
Publication date: 2025/12/04
Petzold FriederikeJeanpierre CécileChen XiaoyiMorinière VincentBenmerah AlexandreDorval GuillaumeSaei HassanHeidet LaurenceAntignac CorinneSaunier Sophie - This study examined therapeutic potential of mitochondrial transplantation using PN-101, a mitochondria preparation derived from human umbilical cord mesenchymal stem cells (UCMSCs), to address SSBP1-related mitochondrial DNA (mtDNA) depletion syndrome. Patient-derived fibroblasts harboring a heterozygous SSBP1 mutation (c.272G＞A:p.Arg91Gln) were treated with PN-101. Its successful uptake and integration into these cells were confirmed. Subsequent analyses revealed that PN-101 treatment significantly increased mtDNA copy numbers in a time- and dose-dependent manner, elevated the expression of key oxidative phosphorylation proteins, and enhanced overall mitochondrial bioenergetics. Taken together, these results provide strong evidence that mitochondrial transplantation holds promise as a therapeutic strategy for primary mitochondrial diseases, including those involving SSBP1 mutations. - Source: PubMed
Publication date: 2025/11/20
Kim DoheeLee Seo-EunCha JuHyuenLee Jun HoKang Young CheolLee Sang-Yeon - Brain metastasis, a leading cause of death in patients with lung adenocarcinoma (LUAD), arises from tumor cells adapting to the unique microenvironment of the brain through metabolic remodeling regulated by key oncogenes. Here, we aimed to determine the role of high mobility group protein box 3 (HMGB3) in regulating tumor cell metabolism to promote the progression and brain metastasis of LUAD. - Source: PubMed
Publication date: 2025/11/05
Cui HuanhuanYang YuechaoLi SenHao YanFeng MingtaoZhou ChangshuaiChen XinGao YangChen LeiWu XiaojunHu WeiguoLi LiangdongCao Yiqun