Ask about this productRelated genes to: UQCRC1 Blocking Peptide
- Gene:
- UQCRC1 NIH gene
- Name:
- ubiquinol-cytochrome c reductase core protein 1
- Previous symbol:
- -
- Synonyms:
- D3S3191, QCR1, UQCR1
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-09
- Date modifiied:
- 2017-09-12
Related products to: UQCRC1 Blocking Peptide
Related articles to: UQCRC1 Blocking Peptide
- Mitochondrial proteases are essential for mitochondrial protein import and constitute the core of the organelle's intrinsic protein quality control system. However, their physiological functions across tissues, as well as their influence on cytosolic proteostasis, remain incompletely understood. - Source: PubMed
Publication date: 2026/06/19
Shi KexinLiu HaoXu HongShang WeinaWang LiquanTong Chao - 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 - Brominated flame retardants (BFRs) are persistent pollutants with health concerns, yet their molecular mechanisms in the inflammatory bowel disease (IBD) and colorectal cancer (CRC) are unclear. - Source: PubMed
Publication date: 2026/06/18
Wu JianhaiLi HaoranWu ChongyingWu YunziYu HuangdaoChen Zhigang - The treatment of keloids (KD) remains challenging. This study focuses on the interplay between mitochondrial dynamics with programmed cell death (PCD) mechanisms in KD. - Source: PubMed
Publication date: 2026/05/10
Li SuyueWei FengZhang LihuaWang MengqiJin YumeiLi Yanling - Tauopathies are neurodegenerative disorders characterized by intracellular accumulation of abnormal tau encoded by , yet their molecular mechanisms remain incompletely understood. We aimed to identify proteomic signatures associated with the primary tauopathies corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP), as well as the secondary tauopathy Alzheimer's disease (AD), and to characterize their interaction networks. Total homogenates from the specified cortical region of postmortem brains of AD ( = 4), CBD ( = 4), PSP ( = 4), and control ( = 4) subjects were analyzed by mass spectrometry (MS). Differentially expressed proteins were subjected to functional enrichment and protein-protein interaction (PPI) network analyses. Reproducibility was assessed using JESS-based western blotting (WB), and selected candidates were examined by immunohistochemistry (IHC) and single-nucleus RNA sequencing (snRNA-seq) to evaluate cell-type-specific transcriptomic profiles. In the four-group comparison, 859, 114, 6, and 1 proteins showed < 0.05, < 0.01, < 0.005, and < 0.001, respectively. Six proteins (AK3, ATP5PD, COX7C, PPA1, PREP, and UQCRC1) with < 0.005 formed a highly interconnected network enriched for mitochondrial pathways, including oxidative phosphorylation and respiratory electron transport. WB validation showed strong concordance for four proteins (AK3, PREP, PPA1, and ATP5PD). IHC confirmed neuronal expression of PPA1 and PREP and revealed prominent microglial PPA1 immunoreactivity in PSP brains. snRNA-seq provided complementary cell-type-specific transcriptomic alterations. These findings suggest mitochondria-associated molecular changes shared across primary and secondary tauopathies; however, given the exploratory nature of this study, these observations should be interpreted cautiously and considered hypothesis-generating, warranting further investigation. - Source: PubMed
Publication date: 2026/05/22
Jannah Alfi RaudatilHasegawa MaiHam JonathanHara NorikazuTsukie TamaoObinata AiKikuchi MasatakaKasuga KensakuYamaguchi HaruyasuHamasaki HideomiTada MariKakita AkiyoshiMatsumoto MasakiMiyashita AkinoriIkeuchi Takeshi