PDCD5 , 1_125aa, Human, Recombinant, E.coli
- Known as:
- PDCD5 , 1_125aa, Human, Recombinant, E.coli
- Catalog number:
- PDC0802
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- PDCD5 1_125aa Human Recombinant .coli
Related genes to: PDCD5 , 1_125aa, Human, Recombinant, E.coli
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- Gene:
- PDCD5 NIH gene
- Name:
- programmed cell death 5
- Previous symbol:
- -
- Synonyms:
- TFAR19, MGC9294
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-10
- Date modifiied:
- 2014-11-19
Related products to: PDCD5 , 1_125aa, Human, Recombinant, E.coli
Related articles to: PDCD5 , 1_125aa, Human, Recombinant, E.coli
- Approximately 10% of eukaryotic proteins are folded by the TRiC/CCT complex (TCP1-ring complex, also called CCT for cytosolic chaperonin containing TCP1), and only open-state TRiC can bind with programmed cell death 5 (PDCD5). However, the physiological role of the PDCD5-TRiC interaction remains elusive. Here, we show that PDCD5 is required for flagellum biogenesis and ciliogenesis and present the PDCD5-TRiC structures in their open states at near-atomic resolution. Mechanically, we find that PDCD5 promotes substrates release by competing with PhLP2A to interact with TRiC, and the depletion of PDCD5 traps flagellum- and cilium-associated proteins within TRiC, finally leading to malformed flagella of spermatids and cilia in mouse ciliated cells. Moreover, we demonstrate that the function of PDCD5 in flagellum biogenesis and ciliogenesis depends on the interaction with TRiC by its C terminus. These findings identify PDCD5 as a TRiC regulator to promote a subset of proteins release. - Source: PubMed
Publication date: 2026/01/07
Wei HuafangSong QianqianWang LiyingDeng QiongWu BingbingChen YinghongHan TingtingGuo YueshuaiLi ZuyangDong FuchengMa ShuangZhao QiaoyuShi XiangyiPan ChenJiang WanyingLiu XiaofeiChen YingyuJiao RenjieYuan LiLiu ChaoGuo XuejiangCong YaoLi Wei - Airway epithelial injury plays a critical role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Mitochondrial dysfunction is implicated in this injury, while the underlying mechanism remains incompletely understood. RNA sequencing was conducted to identify key genes involved in mitochondrial dysfunction in airway epithelial injury induced by cigarette smoke extract (CSE). We identified 1981 significantly up-regulated and 4952 down-regulated differentially expressed genes (DEGs) in CSE-treated airway epithelial cells. A protein-protein interaction network constructed from the DEGs revealed that several key genes were involved in CSE-induced airway epithelial injury. Additionally, PDCD5 was identified as a hub gene potentially linked to mitochondrial dysfunction. PDCD5 expression was significantly increased in the airway epithelium of COPD patients and the corresponding experimental mice. The mRNA and protein expression levels of PDCD5 were significantly increased in concentration- and time-dependent manners in airway epithelial cells treated with CSE. PDCD5 silencing significantly attenuated CSE-induced mitochondrial reactive oxygen species (ROS) accumulation, mitochondrial membrane potential loss, and intracellular ATP depletion. Transmission electron microscopy revealed that PDCD5 siRNA treatment ameliorated CSE-induced mitochondrial structural damage. Moreover, PDCD5 knockdown significantly reduced intracellular ROS accumulation, attenuated apoptosis increases, and inhibited cell viability decline in airway epithelial cells treated with CSE. Our findings demonstrate that PDCD5 contributes to airway epithelial cell damage through the mitochondrial pathway and participates in the pathogenesis of COPD, implicating it as a potential diagnostic biomarker and therapeutic target for COPD. - Source: PubMed
Publication date: 2025/12/25
Shan HuZhang RuiLi Yu-ErLi RuiGe Shao-BoLiu JinYao Shi-YuanYang XiaZhang TaoZhang Ming - Current organoid culture systems face critical limitations: standardized growth factor formulations fail to capture patient-specific signaling requirements, while single-cell-type approaches overlook tumor-stromal interactions essential for understanding immunotherapy resistance. To address these challenges, we developed an automated biofabrication platform that systematically integrates patient-derived three-dimensional (3D) cultures with comprehensive growth factor profiling across 128 combinations. Through rigorous optimization of Matrigel concentration and gelation kinetics, we established standardized conditions achieving uniform signal distribution and quantitative reproducibility. Screening of 23 ovarian cancer patient samples identified universal growth factor combinations that consistently promoted robust cell growth while preserving parental tumor characteristics. Integration of growth factor response profiles with multi-scale genomic analysis revealed two estradiol-responsive cellular populations coordinating immunosuppression: a malignant cell fraction (MAL.PDCD5) that suppresses immune infiltration and a cancer-associated fibroblast fraction (FB.TNFSF10) that promotes immune exclusion through enhanced TGF-signaling. Spatial transcriptomic validation demonstrated striking mutual exclusivity between FB.TNFSF10 cells and T/NK cells in native tissue architecture. Most significantly, FB.TNFSF10 abundance emerged as a robust predictor of immune checkpoint inhibitor therapy resistance across multiple cancer cohorts, independent of conventional biomarkers. This biofabrication platform provides a scalable, reproducible framework with broad applicability beyond oncology. The systematic optimization methodology is readily adaptable to other tissue types, disease models, and high-throughput drug screening applications, representing a significant advancement in functional tissue engineering for precision medicine. - Source: PubMed
Publication date: 2025/12/11
Lee KwanghwanKim MinsungLim Si OnShin Dong-JuShin YunChoi Jung-JooLee MariaKang Hyun JuLee Jeong-WonLee Jin-Ku - Cardiomyopathy often results in heart failure and mortality, significantly impairing patients' quality of life. Advancements in genomics and proteomics now enable the identification of proteins associated with cardiomyopathy, offering valuable insights for its diagnosis and treatment. However, numerous potential pathogenic proteins remain unidentified, underscoring the need for further exploration of novel drug targets for cardiomyopathy. This study aims to employ Mendelian randomization (MR) to explore genetic associations between plasma proteins and cardiomyopathies, with the objective of identifying potential drug targets. Two-sample MR was employed to investigate causal relationships between cardiomyopathies and plasma proteins, using summary data from genome-wide association studies of different cardiomyopathy subtypes, such as dilated cardiomyopathy, hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy (RCM). Cis-protein quantitative trait loci retrieved from the deCODE database served as genetic instruments. Steiger filtering was applied to assess and validate reverse causality. Enrichment analysis was conducted to elucidate potential biological effects, while protein-protein interaction networks were examined to explore interactions among proteins. Molecular docking was employed to evaluate the binding affinity between drugs and their targets. The MR analysis identified 70 significant proteins linked to cardiomyopathy, 12 to dilated cardiomyopathy, 60 to HCM, and 103 to RCM. Intersection analysis revealed 24 significant proteins. Following multiple hypothesis testing, 2 significant proteins (CCL17, SERPINA4) were identified for HCM, and 16 significant proteins (APOL3, C1QL1, CNDP1, CRLF1, CSF2RB, CTSH, GABARAPL2, GP1BA, ICAM5, NPPB, NTM, PDCD5, PTPRS, RNASET2, RTN4R, TCN2) were identified for RCM. Reverse causality testing provided no evidence of reverse causality for any positive genes. Enrichment analysis of protein-protein interaction networks indicated a potential biological role for the positive proteins. Moreover, potential drug targets for treating cardiomyopathy were identified. The genetic associations between plasma proteins and cardiomyopathy were analyzed, leading to the identification of specific proteins as potential biomarkers. Additionally, novel drug targets were identified, providing valuable insights for the diagnosis and treatment of cardiomyopathy. - Source: PubMed
Ji YandiDai GuohuaFan MaoxiaChen ChenLiu RuixiaDong XueyanGao Wulin - This investigation explored the chemopreventive effects of eugenol on diethylnitrosamine (DENA) and acetylaminofluorene (AAF)-induced hepatocellular carcinoma (HCC) in Wistar rats. To induce HCC, DENA was administered intraperitoneally once per week for two weeks at a concentration of 150 mg/kg body weight (b.w.), followed by oral AAF administration for 3 weeks, four times a week, at a dosage of 20 mg/kg b.w. After these three weeks, the rats were treated with eugenol every other day for 17 weeks at a dosage of 20 mg/kg b.w. In vitro, eugenol reduced cell viability (IC50 of 189.29 µg/mL) and inhibited cell migration in the HCC cell line HepG2. Moreover, eugenol treatment in DENA/AAF-induced rats significantly improved cancerous histopathological changes and reduced inflammatory cell infiltration in the liver. Eugenol treatment significantly reduced the activity levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP), along with the levels of total bilirubin (TBIL), alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA 19-9), lipid peroxides (LPO), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). Additionally, the expressions of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), interleukin-8, C-X-C Motif Chemokine Receptor 3 (CXCR3), B-cell lymphoma 2 (Bcl-2), IQ Motif Containing GTPase Activating Protein 1 (IQGAP1), IQ Motif Containing GTPase Activating Protein 3 (IQGAP3), Harvey rat sarcoma viral oncogene homolog (HRAS), Kirsten rat sarcoma viral oncogene homolog (KRAS), and Ki-67 were downregulated following eugenol administration in DENA/AAF-induced HCC. Conversely, eugenol supplementation significantly enhanced glutathione (GSH) content, as well as the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD), and the levels of nuclear factor erythroid 2-related factor 2 (Nrf2). Furthermore, the expressions of tumor suppressor gene p53, Bcl-2-associated X protein (BAX), death receptor 4 (DR4), death receptor 5 (DR5), decoy receptor 1 (DcR1), programmed cell death 5 (PDCD5), and IQ Motif Containing GTPase Activating Protein 2 (IQGAP2) were markedly upregulated compared to the DENA/AAF-administered group. These findings indicate that the potent anticancer effects of eugenol are primarily driven by its ability to reduce oxidative stress, suppress inflammation, and inhibit cell proliferation while promoting apoptosis. This study underscores the potential of eugenol as a promising therapeutic agent for the prevention and management of HCC, offering a novel approach to HCC treatment. - Source: PubMed
Publication date: 2025/06/12
Zaky Mohamed YMorsy Hadeer MAbdel-Moneim AdelZoheir Khairy M ABragoli AnthonyAbdel-Maksoud Mostafa AAlamri AbdulazizAhmed Osama M