Ask about this productRelated genes to: FKBP8 antibody
- Gene:
- FKBP8 NIH gene
- Name:
- FKBP prolyl isomerase 8
- Previous symbol:
- -
- Synonyms:
- FKBP38, FKBPr38
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-28
- Date modifiied:
- 2018-11-01
Related products to: FKBP8 antibody
Related articles to: FKBP8 antibody
- ARID1A loss has been shown to promote the development and progression of cancers by modulating different target genes, including microRNAs (miRs). This study was performed to identify ARID1A-regulated miRs involved in esophageal cancer progression. - Source: PubMed
Publication date: 2026/02/26
Liao HongliRen ChunyiJiang YiWang FengxiangDai Yanyan - () is well-known for its remarkable adaptability to environmental stress and its capacity for rejuvenation The current study was undertaken to identify an upstream cue that senses stress changes in the external milieu and governs a binary fate decision to maintain dormancy or unlock regeneration. We performed proteome-scale profiling across the cyst and early stolon stages of sp., with an emphasis on extracellular signaling and translational control. Proteome dynamics from the cyst to early stolon stage converge on a coherent "sensor-to initiation" architecture, including a sensor layer (TRP/PIEZO mechanotransducers, purinergic receptors, and integrin/FAK), an initiation layer (mTORC1-eIF4F signaling), and a stress-modulation layer (PERK-ISR signaling). We also nominate three actionable upstream hubs whose changes could be sufficient, in principle, to create a pro-translation state: CUL3-Kelch adaptors, Rag GTPase regulators and FKBP8-linked quality-control nodes. We therefore we propose a compact, testable mechanism for regeneration commitment in which sensor-integrated cues drive a calibrated mTORC1-eIF4F "initiation switch" buffered by a protective ISR. The identification of CUL3-Kelch, Rag GTPases, and FKBP8 as leverage points yields immediate hypotheses for transiently unlocking initiation to hasten repair. - Source: PubMed
Publication date: 2026/03/30
Liu ShuangTakemasa ErikaMogi Masaki - The application of platinum-based chemotherapy is often limited by drug resistance, which involves multiple signalling pathways. Although the sulfonamide anticancer agent indisulam has been utilised as an adjuvant in combination with cisplatin, olaparib, and temozolomide in clinical trials, the mechanism by which indisulam modulates the sensitivity of gastric cancer cells to these drugs remains elusive. Here, flow cytometry, TUNEL, and CCK-8 assays demonstrated that indisulam induced apoptosis in gastric cancer cells and enhanced their sensitivity to cisplatin and oxaliplatin. Label-free quantitative proteomics identified FKBP8 as a previously undescribed downstream target of indisulam in gastric cancer cells. qPCR analysis of clinical samples revealed a strong correlation between the mRNA levels of FKBP8 and RBM39, and Kaplan-Meier plot analyses indicated that high expression of FKBP8 mRNA was associated with reduced survival time for gastric cancer patients. Mechanistically, indisulam attenuated FKBP8 transcription, and depletion of FKBP8 enhanced apoptosis and reduced colony formation in the presence of cisplatin and oxaliplatin, thereby improving the chemotherapeutic response of gastric cancer cells to these drugs. FKBP8 overexpression abrogated the effect of indisulam and cisplatin on apoptosis and cell proliferation. Experiments using a xenograft mouse model further demonstrated that the combination of indisulam and cisplatin significantly inhibited the growth of gastric cancer cells, reduced FKBP8 mRNA levels, and increased apoptosis. Taken together, this and previous studies suggest that indisulam can inhibit viability and migration, but promote apoptosis of gastric cancer cells through distinct downstream targets, suggesting that FKBP8 could be leveraged as a therapeutic target in combination with chemotherapy for gastric cancer. - Source: PubMed
Publication date: 2026/03/20
Li YueLu ChengpiaoLu JiaqiJiang HonglvLi DanWang YuhongXu GuoqiangWang XiaohuiMa Jingjing - Mitochondrial dynamics, orchestrated by a finely tuned balance between fusion and fission, are critical for cellular homeostasis and development. Dysregulation of these processes has been increasingly implicated in various diseases, including developmental disorders. Although core components, such as mitofusin 1 and 2 (MFN1/2), have been characterized, the broader regulatory network remains incompletely defined. - Source: PubMed
Publication date: 2026/03/10
Na DoHyeongYoo SeungminJeong MuhahLee NahyunKim YoungwonKim YoubinCho Dong-HyungJung Yong-Keun - Immune checkpoint inhibitors (ICIs) have revolutionised cancer treatment and patients' survival. However, ICIs also cause severe immune-related adverse events, notably colitis, resulting in ICIs therapy discontinuation and tumour immunotherapy failure. This study investigates long myosin light chain kinase 1 (MLCK1), a known regulator of tight junction and gut permeability, to elucidate the mechanisms underlying ICI-mediated colitis and identify approaches to reduce this toxicity. - Source: PubMed
Publication date: 2026/01/06
Xiong LeiHuang JianshangDong YunshengHan WeiKuo Wei-TingXu WentaoHan YiranAn ChenchenZhu RumengZhu NinaXia HanqiRahman AbduxukurTang SainanJiang ChongguiZhao JunhaoPei WangxiangWang JuanWang XiandaSong JiayiWang ZihanWu ShanshanZhang HuiXu HonghaiWu BaomingHuang QianshengBao BinMei QiaoZhu HuaqingHou LanlanLiangpunsakul SuthatCao FengWeng HongleiTan BeiTurner Jerrold RWang HuaZuo Li