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
- Platinum-based chemotherapeutic agents display broad-spectrum and high anticancer activity, the primary target of which is nuclear DNA. During platinum chemotherapeutics, the steady-state levels of reactive oxygen species (ROS) are generally elevated. However, the pathways by which platinum drugs generate ROS and the biological responses still lack systematic studies. Taking carboplatin as an example, we found that both ROS and antioxidant enzyme expression were elevated, and multiple genes for mitochondrial translation and respiration were up-regulated to serve as contributors to ROS. Various genes for mitoribosome stress were also up-regulated, potentially controlling mitochondrial respiration and translation. The expression of single‑stranded DNA‑binding protein 1 (SSBP1), a mitochondrial translational regulator and a potential anti‑cancer target, was up‑regulated in carboplatin-treated cancer cells and in 22 tumor tissues, probably influencing the efficacy of chemotherapy. The potential crosstalk between mitochondrial translation and ROS response should be crucial for the clinical use of platinum drugs. - Source: PubMed
Li QinQin SiYang LiuxinLi ManLi Xiang - The mechanisms responsible for pulmonary fibrosis remain incompletely understood. This study investigated the effect of alpha1,2-fucosylation deficiency on bleomycin-induced pulmonary fibrosis using wild-type C57BL/6J mice and Fut1/Fut2/Sec1 triple-knockout mice deficient in alpha1,2-fucosylation. Mice were treated with bleomycin, and lung tissues and bronchoalveolar lavage fluid (BALF) were collected on Day 7 and Day 14. DFTKO mice showed improved survival and attenuated histological lung injury and collagen deposition compared with WT mice. BALF samples were analyzed by TMT 10-plex quantitative proteomics using 18 individual samples, with three biological replicates per genotype/time-point group. Differentially expressed proteins were prioritized using combined criteria of fold change ≥1.2 or ≤0.83, P < 0.05, and VIP score >1. In WT mice, multiple bronchoalveolar lavage proteins were elevated 7 days after bleomycin treatment, including 1) proteins involved in lipid metabolism, antimicrobial defense and inflammation: BPIFA2 (FC = 25.04, VIP = 1.22, P = 0.01), APOA1(FC = 8.37, VIP = 1.23, P = 0.02), C1QTNF5(FC = 7.72, VIP = 1.20, P = 0.049), SERPINA3N(FC = 6.64, VIP = 1.22 P = 0.4); 2) proteins involved in TGF-beta and extracellular matrix signaling: FST(FC = 14.28, VIP = 1.23, P = 0.02), BGN(FC = 13.58, VIP = 1.20, P = 0.02), TIMP1(FC = 10.72, VIP = 1.21, P = 0.04), VCAN(FC = 9.04, VIP = 1.21 P = 0.00008); 3) Collagens: COL5A1(FC = 9.63, VIP = 1.22 P = 0.01), COL5A2(FC = 7.09, VIP = 1.19 P = 0.03). Several proteins involved in detoxification of reactive oxygen species (ROS) were found to be decreased 7 days after bleomycin treatment: SELENBP1(FC = 0.18, VIP = 1.22, P = 0.02), GLRX5(FC = 0.18, VIP = 1.23, P = 0.02), UQCRC1(FC = 0.17, VIP = 1.23, P = 0.0005). In the Day 7 comparison between DFTKO and WT mice, proteins related to DNA damage repair, genome stability, wound healing, and tissue remodeling were increased in DFTKO mice, including H3C1 (FC = 3.66, VIP = 1.68, P = 0.03), SSBP1(FC = 2.96, VIP = 1.78, P = 0.0004), HMGA1(FC = 2.84, VIP = 1.60, P = 0.01), HDGFL3(FC = 3.97, VIP = 1.66, P = 0.01) and CEACAM1(FC = 2.93, VIP = 1.65, P = 0.006). These data suggest α1,2-fucosylated glycans as potential therapeutic targets for pulmonary fibrosis. Lack of alpha1,2 fucosylated structures attenuates bleomycin-induced lung fibrosis, while exact mechanisms will be focus of our future study. - Source: PubMed
Publication date: 2026/06/18
Zhu ChenxiJiang YichengMai XinjiaJi ZhaohuiAbdylla GulberdiyevZhou Dapeng - 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
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