Ask about this productRelated genes to: TBK1 Blocking Peptide
- Gene:
- TBK1 NIH gene
- Name:
- TANK binding kinase 1
- Previous symbol:
- -
- Synonyms:
- NAK
- Chromosome:
- 12q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-08
- Date modifiied:
- 2019-04-23
Related products to: TBK1 Blocking Peptide
Related articles to: TBK1 Blocking Peptide
- Hydroxycinnamic acids (HCAs), specifically cinnamic, caffeic, and ferulic acids, are core bioactive components of traditional Chinese medicinal herbs such as Cinnamomi Cortex (Cinnamomum aromaticum Nees) and Asafoetida (Ferula assa-foetida L.), used for regulating metabolic disorders and inflammation. Despite their widespread clinical application, their specific molecular targets remain unidentified. - Source: PubMed
Publication date: 2026/05/23
Ma XiaojingWang JiamingGuo YakunNan YananGuo LinyueWang YajingJiang MiaoYang MingruiMa Wenfu - Low back pain (LBP) is a highly prevalent musculoskeletal disorder worldwide. Nucleus pulposus cell (NPC) pyroptosis contributes to intervertebral disc degeneration (IVDD), but the underlying mechanisms remain unclear. We identified TMEM2, a transmembrane protein not previously linked to IVDD, as markedly upregulated in degenerated NPCs by single‑cell RNA sequencing. TMEM2 expression correlated positively with IVDD severity and NPC pyroptosis, and its knockdown alleviated pyroptosis. Mechanistically, TMEM2 binds BAX to promote mPTP opening, leading to mtDNA release and activation of the STING-TBK1-NF‑κB pathway, ultimately triggering NLRP3 inflammasome‑mediated pyroptosis. To address the avascular nature of the disc, we developed an injectable ROS‑responsive hydrogel microsphere system encapsulating shTMEM2‑loaded liposomes (Lipo/shTMEM2@MS). This platform enables sustained release, on‑demand degradation, and single‑dose intradiscal administration. In a rat model, Lipo/shTMEM2@MS effectively ameliorated disc degeneration. Collectively, these findings identify TMEM2 as a key driver of NPC pyroptosis and establish a ROS‑responsive microsphere strategy as a promising translational approach for IVDD. - Source: PubMed
Publication date: 2026/05/22
Xu ZhiqiangFang HanmoPeng ChengruiLiao ZhiweiYang GuoyuQian HuAo JunWu Xinghuo - Pancreatic cancer is a highly aggressive malignancy with a poor prognosis, primarily due to its immunosuppressive tumor microenvironment (TME) and suboptimal efficacy of current immunotherapies. Herein, we developed a novel conjugate (LNT-DMXAA) by covalently grafting the STING agonist DMXAA onto the immunomodulatory polysaccharide (lentinan, LNT) via esterification and Schiff-base reactions, showing high drug loading (DMXAA, 9.91%; LNT, 90.09%) and enzyme/pH-responsive drug release. In vitro experiments revealed that LNT-DMXAA effectively elicited STING-dependent BMDC maturation via the TBK1-IRF3 axis, upregulating IFN-β and CXCL10, and exhibiting negligible cytotoxicity. Additionally, DMXAA synergized with LNT to enhance BMDC activation and OVA antigen presentation, with LNT-DMXAA demonstrating greater effectiveness. In Pan02 mice, LNT-DMXAA significantly inhibited tumor growth by activating dendritic cells for antigen presentation, promoting intratumoral CD8/CD4 T-cell infiltration, and performed better than DMXAA, LNT and physical mixtures. In addition, the conjugate exhibited excellent biocompatibility without notable organ toxicity or hemolysis, while enhancing DMXAA solubility. Collectively, LNT-DMXAA demonstrates potential as a pancreatic cancer immunotherapy agent by integrating LNT and DMXAA to synergistically address tumor immune evasion. - Source: PubMed
Publication date: 2026/05/21
Zhang ZhengxianZhu XinCui JingruHan JialeWang JiaxingZhou HuijieWu XiangxiangZeng Huahui - Fucoxanthin (FX), a natural carotenoid derived from marine brown algae, possesses extremely high anti-inflammatory activity. However, the precise mechanisms underlying its protective effects against stomatitis remain to be elucidated. This study aimed to explore the protective effects and mechanisms of FX in the treatment of stomatitis. Histopathological examination was conducted on oral mucosal tissues from rats with 5-fluorouracil (5-FU)-induced oral mucositis. Western blotting and immunofluorescence staining were used to explore the epithelial-mesenchymal transition (EMT), tight junction proteins, mitochondrial function, mitochondrial autophagy and the expression of key molecules involved in the cGAS-STING signaling in HOKs. Moreover, molecular docking analysis was applied to predict the binding interactions between FX and cGAS/STING proteins. The results showed that FX markedly alleviated the symptoms of whitening and swelling of the oral mucosa and thinning of the epithelium in 5-FU-induced rats. In LPS-induced HOKs, FX restored the abnormal localization of Occludin and ZO-1 proteins, ameliorated mitochondrial dysfunction, and inhibited EMT. Furthermore, the protein levels of cGAS, STING, and TBK1 were downregulated by FX treatment. Molecular docking revealed direct binding between FX and both cGAS and STING. Collectively, these findings indicate that FX may alleviate LPS-induced stomatitis by ameliorating mitochondrial dysfunction to reduce mitochondrial DNA (mtDNA) release, thereby inhibiting the cGAS-STING signaling pathway. These results suggest that FX holds promise as a therapeutic candidate for stomatitis. - Source: PubMed
Publication date: 2026/05/21
Lin CaipengDeng LiliXie XiLuo Hai-BinLiu Deyu - KRAS is mutationally activated in 45%-50% of colorectal cancer (CRC) cases, and while KRAS-targeted therapies have shown clinical promise, drug resistance limits their efficacy. To explore the mechanisms underlying KRAS inhibitor resistance, we use targeted exome sequencing and spatial transcriptomics on patient-matched CRC biopsies following combined treatment with KRAS and EGFR inhibitors. We show that acquired genetic events are identified in most patients at progression but are often subclonal and coexist with transcriptional adaptive states. Mesenchymal, YAP, and fetal-like transcriptional signatures predominate in resistant tumors, while inflammatory programs are induced early on treatment. Single-cell spatial analysis reveals intratumoral heterogeneity, with diverse adaptive states in different zones of individual tumors. Using human and murine organoid models, we show that drug-induced inflammatory programs are, at least in part, cancer-cell autonomous, and precede the emergence of drug resistance. We identify TBK1 as a target to abrogate the inflammatory adaptive phase and enhance responses to KRAS inhibition. - Source: PubMed
Publication date: 2026/05/21
Alonso SalvadorChu KevanGranowsky ElizabethRabanales Valeria SaraibaParsons Marie JGunasinghe HimariShia JinruYaeger RonaDow Lukas E