Ask about this productRelated genes to: FKBP8 Blocking Peptide
- 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 Blocking Peptide
Related articles to: FKBP8 Blocking Peptide
- The translocase of the outer mitochondrial membrane (TOM) is the conserved entry gate for nuclear-encoded proteins. While structurally similar from yeast to humans, the human TOM complex operates in a cellular environment of vastly greater complexity. Here, we present a high-confidence map of the human TOM interactome using a membrane-permeable cross-linker to capture both stable and transient interactors. Alongside extensive overlap with known yeast partners, we uncover a set of human-specific interactors including regulatory factors and TOM-associated proteins. Mapping unique interprotein cross-links reveals conformational flexibility of the receptor TOM20 and enhanced recovery of peripheral components such as TOM70 and several associated quality control factors. Notably, we identify FKBP8 (FK506 binding protein 8) as a human-specific interactor that binds multiple TOM subunits and promotes organization of the complex. Our work redefines the human TOM complex as a dynamic, multifaceted hub coordinating biogenesis, quality control, and signaling. This expanded TOM landscape offers a rich resource for exploring mitochondrial regulation in health and disease. - Source: PubMed
Publication date: 2026/05/01
Borrero-Landazabal Mayra ALinke VanessaKadavá TerezaLi ZeshiDraczkowski PiotrKaszuba KacperBertgen LeaSerwa Remigiusz AHeck Albert J RChacinska Agnieszka - 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