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Contact NowTAR DNA binding protein 43 kDA (TDP-43) is a highly conserved and ubiquitously expressed RNA/DNA binding protein belonging to the heterogeneous nuclear ribonucleoprotein (hnRNP) family. The dysfunction of TDP-43-related pathways is increasingly recognized as an important pathogenic mechanism in neurodegenerative diseases. In 2006, hyperphosphorylated and ubiquitinated TDP-43 cytoplasmic inclusions were identified as pathological features of amyotrophic lateral sclerosis (ALS) and frontotemporal lobe disease (FTLD). In these pathological deposits, TDP-43 undergoes numerous post-translational modifications (PTM), including polyubiquitination, hyperphosphorylation, and protein hydrolytic cleavage.
Fig. 1. Putative mechanisms by which TDP-43 exerts its pathogenic effects in TDP-43 proteinopathies. (Boer EMJ, et al., 2020)
TDP-43 has been shown to undergo liquid-liquid phase separation (LLPS) in vitro and some of its functions are closely related to its ability to phase separate. TDP-43 mutations are associated with a growing number of neurodegenerative diseases. CD BioSciences offers specialized services to analyze LLPS of TDP-43 in neurodegenerative diseases.
We can analyze neurodegenerative diseases associated with TDP-43 and link these diseases to the structure and function of TDP-43 by detecting related genes.
Neurodegenerative Diseases Associated with TDP-43 | Related Genes |
Classical Amyotrophic Lateral Sclerosis | ALS2, SETX, TARDBP, VAPB, ANG, UBQLN2, OPTN, PFN1, UNC13a, NEK1, C21orf2, SIGMAR1, DCTN1, MATR3, VCP, hnRNPA1/A2b1, NIPA1, TBK1, ATXN2, UBQLN2, SQSTM1 |
ALS-FTLD, ALS-ci/bi | TARDBP, CHMP2b, TBK1, UBQLN2, SQSTM1, DCTN1, UNC13a |
FTLD | CHMP2b, GRN, SQSTM1, OPTN, TBK1, ATXN2 |
Perry Disease | DCTN1 |
Facial Onset Sensory and Motor Neuronopathy (FOSMN) | SOD1, SQSTM1, VCP, CHCHD10 |
Importantly, our team of experts is dedicated to developing therapeutic strategies for TDP-43 protein disease by removing TDP-43 protein aggregates and modulating other TDP-43 pathogenic processes. We offer cutting-edge in vivo, computer and cellular experiments to analyze the key molecular pathways of TDP-43-induced neurodegeneration, including:
Furthermore, we systematically integrate these regulatory approaches with proteomic, transcriptomic, imaging, genetic, and epidemiological data to explore the pathogenesis of abnormal phase changes in TDP-43 and to develop potential therapeutic targets to prevent and treat these neurodegenerative diseases.
CD BioSciences aims to analyze the relationship between the genetic and molecular processes involved in TDP-43 dysfunction to help our clients develop therapeutic targets and novel biomarkers for the treatment of ALS and FTLD. If you are interested in our services, please feel free to contact us.
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