mProX™ Human TTBK1 Stable Cell Line

Yukawa, Kayo. et al. "Antisense oligonucleotide-based targeting of Tau-tubulin kinase 1 prevents hippocampal accumulation of phosphorylated tau in PS19 tauopathy mice." Acta neuropathologica communications, 2023.
Tau tubulin kinase-1 (TTBK1) is a kinase that is primarily found in neurons and is highly expressed in the entorhinal cortex and hippocampal regions. This specific region is where early tau pathology develops in Alzheimer's disease (AD). Studies have shown that TTBK1 levels are increased in the brains of AD patients compared to control subjects. It has been hypothesized that targeting Ttbk1 with antisense oligonucleotide (ASO) could prevent the accumulation of phosphorylated tau, thus slowing the progression of tau pathology in AD. In vivo experiments using ASO to target Ttbk1 in a mouse model of AD showed a specific reduction in Ttbk1 expression in the temporal cortex without affecting Ttbk2 expression. This resulted in a significant reduction of phospho-tau epitopes associated with AD. Immunofluorescence studies also showed a decrease in phospho-tau levels in specific regions of the brain. Further analysis revealed potential interactions with immune processes, specifically interferon-gamma and complement pathways, suggesting a potential effect on microglial activity. These findings demonstrate the potential of TTBK1 as a therapeutic target for reducing pathological tau phosphorylation in the early stages of AD without compromising TTBK2 expression.
Yukawa, Kayo. et al. "Antisense oligonucleotide-based targeting of Tau-tubulin kinase 1 prevents hippocampal accumulation of phosphorylated tau in PS19 tauopathy mice." Acta neuropathologica communications, 2023.
Pubmed: 37853497   DOI: 10.1186/s40478-023-01661-3

Martinez-Gonzalez, Loreto. et al. "TTBK1 and CK1 inhibitors restore TDP-43 pathology and avoid disease propagation in lymphoblast from Alzheimer's disease patients." Frontiers in molecular neuroscience, 2023.
Recent studies have identified TDP-43 proteinopathy as a potential contributor to the development of Alzheimer's disease (AD). Immortalized lymphocyte models from AD patients have revealed an increase in post-translational modifications of TDP-43, including hyperphosphorylation and fragmentation, as well as prionic behavior and intercellular transmission of the disease. To address this phenomenon and improve treatment strategies, various kinase inhibitors are proposed to target this pathological mechanism. This research aims to contribute to the advancement of therapeutic interventions for AD.
Martinez-Gonzalez, Loreto. et al. "TTBK1 and CK1 inhibitors restore TDP-43 pathology and avoid disease propagation in lymphoblast from Alzheimer's disease patients." Frontiers in molecular neuroscience, 2023.
Pubmed: 37621404   DOI: 10.3389/fnmol.2023.1243277