Associated Papers
Clinical Spectrum of TGM6-Related Movement Disorders: A New Report with a Pooled Analysis of 48 Patients.
Sharawat IK et al.
Journal of Neurosciences in Rural Practice, 2021
A case report of late-onset cerebellar ataxia associated with a rare p.R342W TGM6 (SCA35) mutation.
Manini A et al.
Bmc Neurology, 2020
TGM6 L517W is not a pathogenic variant for spinocerebellar ataxia type 35.
Chen Y et al.
Neurology. Genetics, 2020
TGM6 variants in Parkinson's disease: clinical findings and functional evidence.
Chen K et al.
Journal of Integrative Neuroscience, 2020
Mutations in TGM6 induce the unfolded protein response in SCA35.
Tripathy D et al.
Human Molecular Genetics, 2017
Genomic variants reveal differential evolutionary constraints on human transglutaminases and point towards unrecognized significance of transglutaminase 2.
Thangaraju K et al.
Plos One, 2017
28248968 (PubMed )
Supplement: pone.0172189.s003.pdf
The autosomal dominant spinocerebellar ataxias: emerging mechanistic themes suggest pervasive Purkinje cell vulnerability.
Hekman KE et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 2015
Application of next-generation sequencing technologies in Neurology.
Jiang T et al.
Annals of Translational Medicine, 2014
Spinocerebellar ataxia 35: novel mutations in TGM6 with clinical and genetic characterization.
Guo YC et al.
Neurology, 2014
Spinocerebellar ataxia type 35 (SCA35)-associated transglutaminase 6 mutants sensitize cells to apoptosis.
Guan WJ et al.
Biochemical and Biophysical Research Communications, 2013
Transglutaminase 6: a protein associated with central nervous system development and motor function.
Thomas H et al.
Amino Acids, 2013
TGM6 identified as a novel causative gene of spinocerebellar ataxias using exome sequencing.
Wang JL et al.
Brain : a Journal of Neurology, 2010
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