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Chun-Chi Liang

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Articles 18
Citations 2670
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Recent Articles
1.
van Lengerich B, Zhan L, Xia D, Chan D, Joy D, Park J, et al.
Nat Neurosci . 2023 Jan; 26(3):416-429. PMID: 36635496
Loss-of-function variants of TREM2 are associated with increased risk of Alzheimer's disease (AD), suggesting that activation of this innate immune receptor may be a useful therapeutic strategy. Here we describe...
2.
Xia D, Lianoglou S, Sandmann T, Calvert M, Suh J, Thomsen E, et al.
Mol Neurodegener . 2022 Jun; 17(1):41. PMID: 35690868
Background: Genetic mutations underlying familial Alzheimer's disease (AD) were identified decades ago, but the field is still in search of transformative therapies for patients. While mouse models based on overexpression...
3.
Li J, Liang C, Pappas S, Dauer W
Elife . 2020 Mar; 9. PMID: 32202496
Genetic redundancy can be exploited to identify therapeutic targets for inherited disorders. We explored this possibility in DYT1 dystonia, a neurodevelopmental movement disorder caused by a loss-of-function (LOF) mutation in...
4.
Schlepckow K, Monroe K, Kleinberger G, Cantuti-Castelvetri L, Parhizkar S, Xia D, et al.
EMBO Mol Med . 2020 Mar; 12(4):e11227. PMID: 32154671
Triggering receptor expressed on myeloid cells 2 (TREM2) is essential for the transition of homeostatic microglia to a disease-associated microglial state. To enhance TREM2 activity, we sought to selectively increase...
5.
Shin J, Hernandez-Ono A, Fedotova T, Ostlund C, Lee M, Gibeley S, et al.
J Clin Invest . 2019 Aug; 129(11):4885-4900. PMID: 31408437
Deciphering novel pathways regulating liver lipid content has profound implications for understanding the pathophysiology of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Recent evidence suggests that the nuclear envelope is...
6.
Pappas S, Liang C, Kim S, Rivera C, Dauer W
Hum Mol Genet . 2017 Nov; 27(3):407-420. PMID: 29186574
A critical challenge to deciphering the pathophysiology of neurodevelopmental disease is identifying which of the myriad abnormalities that emerge during CNS maturation persist to contribute to long-term brain dysfunction. Childhood-onset...
7.
Yellajoshyula D, Liang C, Pappas S, Penati S, Yang A, Mecano R, et al.
Dev Cell . 2017 Jul; 42(1):52-67.e4. PMID: 28697333
The childhood-onset motor disorder DYT6 dystonia is caused by loss-of-function mutations in the transcription factor THAP1, but the neurodevelopmental processes in which THAP1 participates are unknown. We find that THAP1...
8.
Richter F, Gerstenberger J, Bauer A, Liang C, Richter A
Behav Brain Res . 2016 Oct; 317:536-541. PMID: 27769743
Hereditary generalized dystonia is often caused by a GAG deletion in TOR1A (DYT1) that encodes for the protein torsinA. Although mutation carriers show alterations in neuronal connectivity and sensorimotor deficits,...
9.
Tanabe L, Liang C, Dauer W
Cell Rep . 2016 Sep; 16(12):3322-3333. PMID: 27653693
DYT1 dystonia is a neurodevelopmental disease that manifests during a discrete period of childhood. The disease is caused by impaired function of torsinA, a protein linked to nuclear membrane budding....
10.
Chen S, Wang C, Yeo S, Liang C, Okamoto T, Sun S, et al.
Genes Dev . 2016 Mar; 30(7):856-69. PMID: 27013233
Autophagy is an evolutionarily conserved cellular process controlled through a set of essential autophagy genes (Atgs). However, there is increasing evidence that most, if not all, Atgs also possess functions...