Ask about this productRelated genes to: TBK1 antibody
- 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 antibody
Related articles to: TBK1 antibody
- Xuebijing (XBJ) has demonstrated efficacy in alleviating clinical symptoms in sepsis patients; however, its underlying mechanism requires further investigation. - Source: PubMed
Publication date: 2026/04/23
Meng XiaoyanYan XinmingKan ChenLi HaiquanHan DaheGuo YiXue PengJiang Yuxin - Alveolar echinococcosis (AE) is a lethal parasitic disease that leads to progressive liver fibrosis, a process characterized by the dominance of M2 macrophages in advanced stages. While the compound Biejia-Ruangan tablet (CBRT) has demonstrated efficacy in reversing hepatic fibrosis, its underlying mechanisms in the context of AE-induced fibrosis are not fully understood. This study aimed to investigate the therapeutic potential of CBRT against AE-induced liver fibrosis and to elucidate its mechanisms of action. Serum levels of liver fibrosis markers and cytokines were measured by ELISA. Liver histopathology and collagen deposition were assessed using H&E and Masson's trichrome staining. Apoptosis in GHA1 hepatocytes was evaluated by flow cytometry. Macrophage migration was analyzed via scratch and Transwell invasion assays. The involvement of the STING-TBK1 signaling pathway was examined through western blotting (WB), immunohistochemistry (IHC), immunofluorescence (IF), and quantitative real-time PCR (qRT-PCR). Livers from (.)-infected mice exhibited severe fibrosis accompanied by significant infiltration of M2 macrophages and upregulated expression of STING-TBK1 pathway components (Arg-1, α-SMA, STING, and TBK1). Treatment with CBRT (1 g/kg) markedly attenuated liver fibrosis ( < 0.01) and inhibited the activation of mouse hepatic stellate cells (mHSCs) . CBRT suppressed the activation of HSCs, partly by upregulating IFN-γ, suppressed apoptosis in GHA1 hepatocytes, and improved hepatocyte function. Mechanistically, CBRT activates the STING-TBK1 signaling pathway, which subsequently suppresses the polarization of macrophages toward the M2 phenotype, thereby alleviating fibrogenesis. This study demonstrates that CBRT alleviates hepatic fibrosis by activating the STING-TBK1 signaling pathway. This activation elicits a shift in macrophage polarization from the pro-fibrotic M2 phenotype towards the M1 phenotype, which subsequently suppresses the activation of hepatic stellate cells and alleviates fibrogenesis. These findings reveal a novel immunomodulatory mechanism of CBRT centered on the STING-TBK1 axis, providing both experimental evidence and a theoretical foundation for its potential application in treating hepatic fibrosis associated with AE. - Source: PubMed
Publication date: 2026/04/21
Ma YuyuZhao HuiLiu YumeiMeng MenggenChen JiahuiSun YuqinFan BinZhou XuanTian FengminMa XiuminWang Liang - Glioblastoma (GBM) remains poorly responsive to immunotherapy due to restricted brain delivery and a profoundly immunosuppressive "cold" microenvironment. Here, we report ultrasmall manganese-doped carbon dots enriched with surface amino and carboxyl groups (Mn-CDs) as a self-adjuvanted nanotherapeutic that integrates dual targeting with a synergistic immune cascade. Mn-CDs exploit LAT1-mediated transport to traverse the blood-brain barrier and preferentially accumulate in glioma tissue, while their intrinsic positive surface potential drives mitochondrial tropism via the mitochondrial membrane potential. Once localized to mitochondria, mixed-valence Mn centers catalyze Fenton-like reactions, amplifying oxidative stress and inducing mitochondrial depolarization and ultrastructural disruption. This organelle-localized stress is coupled to robust activation of the cGAS-STING-TBK1-IRF3 axis, leading to elevated IFN-I signaling and proinflammatory chemokine production. In parallel, Mn-CDs elicit immunogenic cell death, as evidenced by calreticulin (CRT) exposure, HMGB1 release, and extracellular ATP emission, thereby promoting dendritic cell maturation and cytotoxic T-cell infiltration. In orthotopic syngeneic GBM models, Mn-CDs remodel the immunosuppressive tumor microenvironment, suppress intracranial tumor progression, and prolong survival with favorable biosafety. Collectively, this work establishes a dual-targeted Mn-based carbon nanoplatform that converts GBM toward an immune-responsive state through convergent cGAS-STING activation and ICD-driven immune priming. - Source: PubMed
Publication date: 2026/03/28
Li ZhenYu ChangshuiChe HongyuXu DuoLu DongWang YanLi XingjunMa ShuoZhang XuZhang ZhengkuiYu Rutong - The blood-brain barrier (BBB) protects the brain but becomes compromised during systemic inflammatory conditions such as sepsis. The mechanisms driving BBB disruption remain incompletely understood. Here, we identified a significant enrichment of the macroautophagy/autophagy-lysosome-related pathway in the upregulated proteome using quantitative proteomics on brain microvessels from mice after cecal ligation and puncture (CLP) that induces polymicrobial sepsis. CLP progressively induced autophagic flux in brain endothelial cells, peaking at 24 h post-procedure before subsiding. Similarly, an mRFP-GFP-LC3 reporter assay and immunoblotting showed that lipopolysaccharide (LPS) treatment increased autophagic flux in bEnd.3 cells in a time- and dose-dependent manner. Mice intraperitoneally (IP) injected with the autophagy inhibitors chloroquine (CQ) or 3-methyladenine (3-MA) were resistant to BBB disruption caused by CLP or IP injection of LPS, whereas those injected with the autophagy inducer rapamycin (Rapa) were more susceptible. CQ and 3-MA reduced, while Rapa increased, CLP-induced lethality in mice. These effects were confirmed using a dextran infiltration assay on bEnd.3 cell transwell cultures. CQ alleviated both the acute disruption of the tight junction proteins TJP1/ZO-1 and CLDN5 in brain microvessels and the long-term memory and anxiety deficits in LPS-challenged mice. siRNA-mediated knockdown of the SNARE protein STX17, which inhibits autophagosome-lysosome fusion, attenuated LPS-induced tight junction protein degradation in bEnd.3 cells. Importantly, inhibition of TLR4 or its downstream kinase TBK1 reduced LPS-induced autophagy and preserved tight junction proteins, implicating TLR4-TBK1 signaling in endothelial autophagy activation. These results suggest that excessive autophagy in endothelial cells drives BBB damage and cognitive dysfunction in sepsis. - Source: PubMed
Publication date: 2026/04/19
Peng MilinChen WeiGao QingtaoZhu XuejingYu LaidongZhang LinZou XinyingHu ZhonghuaZhang Lina - Clear cell renal cell carcinoma (ccRCC) with von Hippel-Lindau (VHL) loss exhibits TBK1 dependency, and targeted therapeutic strategies outside of HIF-2α inhibition have remained limited. In this issue of Cell Chemical Biology, Liao et al. describe a second-generation cereblon-recruiting TBK1 proteolytic targeting chimera (PROTAC) with promising pre-clinical activity. - Source: PubMed
Kwon HyunwooBers Alan EBarbie David A