Associated Papers
Comparison of clinical and imaging features of cerebral small vessel disease associated with heterozygous HTRA1 and NOTCH3 mutations.
Lee YC et al.
International Journal of Stroke : Official Journal of the International Stroke Society, 2026
Rare Variants in HTRA1, SGTB, and RBM12 Confer Risk of Atherosclerotic Cardiovascular Disease Independent of Traditional Cardiovascular Risk Factors.
Lockhart SM et al.
Circulation. Genomic and Precision Medicine, 2025
HTRA1-dependent proteolysis induces age-related retinal degeneration and exacerbates choroidal neovascularization.
Katschke KJ et al.
Disease Models & Mechanisms, 2025
The serine protease HTRA1 targets tau fibrils and provides a proteolytic barrier against pathogenic protein conformations.
Hagemeier B et al.
The Journal of Biological Chemistry, 2025
Synergistic Multi-Pronged Interactions Mediate the Effective Inhibition of Alpha-Synuclein Aggregation by the Chaperone HtrA1.
Chinchilla P et al.
Biorxiv : the Preprint Server for Biology, 2024
Rational correction of pathogenic conformational defects in HTRA1.
Beaufort N et al.
Nature Communications, 2024
HTRA1 disaggregates α-synuclein amyloid fibrils and converts them into non-toxic and seeding incompetent species.
Chen S et al.
Nature Communications, 2024
Genetically proxied HTRA1 protease activity and circulating levels independently predict risk of ischemic stroke and coronary artery disease.
Dichgans M et al.
Research Square, 2023
HtrA1 prevents and reverses α-synuclein aggregation, rendering it non-toxic and seeding incompetent.
Chen S et al.
Research Square, 2023
Inappropriate interpretation of non-pathogenic HTRA1 variant as pathogenic.
Uemura M et al.
Annals of Clinical and Translational Neurology, 2023
High frequency of HTRA1 AND ABCC6 mutations in Japanese patients with adult-onset cerebral small vessel disease.
Uemura M et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 2023
Novel mutations in HTRA1-related cerebral small vessel disease and comparison with CADASIL.
Zhang C et al.
Annals of Clinical and Translational Neurology, 2022
Allosteric inhibition of HTRA1 activity by a conformational lock mechanism to treat age-related macular degeneration.
Gerhardy S et al.
Nature Communications, 2022
An allosteric HTRA1-calpain 2 complex with restricted activation profile.
Rey J et al.
Proceedings of the National Academy of Sciences of the United States of America, 2022
Proteomic profiling in cerebral amyloid angiopathy reveals an overlap with CADASIL highlighting accumulation of HTRA1 and its substrates.
Zellner A et al.
Acta Neuropathologica Communications, 2022
Whole-exome sequencing reveals a role of HTRA1 and EGFL8 in brain white matter hyperintensities.
Malik R et al.
Brain : a Journal of Neurology, 2021
Chromosome 10q26-driven age-related macular degeneration is associated with reduced levels of HTRA1 in human retinal pigment epithelium.
Williams BL et al.
Proceedings of the National Academy of Sciences of the United States of America, 2021
Corrigendum: HTRA1 Mutations Identified in Symptomatic Carriers Have the Property of Interfering the Trimer-Dependent Activation Cascade.
Uemura M et al.
Frontiers in Neurology, 2021
A novel heterozygous HTRA1 mutation is associated with autosomal dominant hereditary cerebral small vessel disease.
Zhuo ZL et al.
Molecular Genetics & Genomic Medicine, 2020
HTRA1 Mutations Identified in Symptomatic Carriers Have the Property of Interfering the Trimer-Dependent Activation Cascade.
Uemura M et al.
Frontiers in Neurology, 2019
AMD-Associated HTRA1 Variants Do Not Influence TGF-β Signaling in Microglia.
Akhtar-Schaefer I et al.
Advances in Experimental Medicine and Biology, 2019
CADASIL brain vessels show a HTRA1 loss-of-function profile.
Zellner A et al.
Acta Neuropathologica, 2018
Characterization of Heterozygous HTRA1 Mutations in Taiwanese Patients With Cerebral Small Vessel Disease.
Lee YC et al.
Stroke, 2018
HtrA1 Mediated Intracellular Effects on Tubulin Using a Polarized RPE Disease Model.
Melo E et al.
Ebiomedicine, 2018
High-Temperature Requirement A1 (Htra1) - A Novel Regulator of Canonical Wnt Signaling.
Globus O et al.
Scientific Reports, 2017
ER stress-induced aggresome trafficking of HtrA1 protects against proteotoxicity.
Gerhardt MJ et al.
Journal of Molecular Cell Biology, 2017
HtrA1 Proteolysis of ApoE In Vitro Is Allele Selective.
Chu Q et al.
Journal of the American Chemical Society, 2016
Heterozygous HTRA1 mutations are associated with autosomal dominant cerebral small vessel disease.
Verdura E et al.
Brain : a Journal of Neurology, 2015
A novel HTRA1 exon 2 mutation causes loss of protease activity in a Pakistani CARASIL patient.
Khaleeli Z et al.
Journal of Neurology, 2015
Age-related macular degeneration-associated silent polymorphisms in HtrA1 impair its ability to antagonize insulin-like growth factor 1.
Jacobo SM et al.
Molecular and Cellular Biology, 2013
Structural and functional analysis of HtrA1 and its subdomains.
Eigenbrot C et al.
Structure (london, England : 1993), 2012
[Clinical manifestations and neuroradiological findings of CARASIL with a novel mutation].
Shibata M
Rinsho Shinkeigaku = Clinical Neurology, 2012
The structural basis of mode of activation and functional diversity: a case study with HtrA family of serine proteases.
Singh N et al.
Archives of Biochemistry and Biophysics, 2011
Cerebral small-vessel disease protein HTRA1 controls the amount of TGF-β1 via cleavage of proTGF-β1.
Shiga A et al.
Human Molecular Genetics, 2011
Substrate-induced remodeling of the active site regulates human HTRA1 activity.
Truebestein L et al.
Nature Structural & Molecular Biology, 2011
The serine protease HtrA1 specifically interacts and degrades the tuberous sclerosis complex 2 protein.
Campioni M et al.
Molecular Cancer Research : Mcr, 2010
Association of HTRA1 mutations and familial ischemic cerebral small-vessel disease.
Hara K et al.
The New England Journal of Medicine, 2009
HtrA1 serine protease inhibits signaling mediated by Tgfbeta family proteins.
Oka C et al.
Development (cambridge, England), 2004
[Two siblings with familial schizencephaly--report of a family and review in relation to clinical features and neuroradiological findings].
Ueda M et al.
Rinsho Shinkeigaku = Clinical Neurology, 1996