Associated Papers
Clonal hematopoiesis associates with prevalent and incident cardiometabolic disease in a cardiac catheterization cohort.
Regan JA et al.
Plos One, 2026
Clonal hematopoiesis in apparent treatment-resistant hypertension, insights from multiple medical centers and community-based cohorts.
Lv C et al.
Nature Aging, 2025
Genome-wide modulation of alternative splicing by a predicted alpha helix in U2AF2.
Xue D et al.
Nucleic Acids Research, 2025
Distinct characteristics of lymphoid and myeloid clonal hematopoiesis in World Trade Center first responders.
Esai Selvan M et al.
Medrxiv : the Preprint Server for Health Sciences, 2025
Clonal Hematopoiesis of Indeterminate Potential Is Associated With Incident Abdominal Aortic Aneurysm.
Tan Y et al.
Arteriosclerosis, Thrombosis, and Vascular Biology, 2025
Clonal hematopoiesis is associated with distinct rheumatoid arthritis phenotypes.
Hiitola E et al.
Science Advances, 2025
Comparative analysis of the Mexico City Prospective Study and the UK Biobank identifies ancestry-specific effects on clonal hematopoiesis.
Wen S et al.
Nature Genetics, 2025
Clonal Hematopoiesis Associates with Prevalent and Incident Cardiometabolic Disease in High-Risk Individuals.
Regan JA et al.
Medrxiv : the Preprint Server for Health Sciences, 2025
Rare variant associations with plasma protein levels in the UK Biobank.
Dhindsa RS et al.
Nature, 2023
Clonal hematopoiesis is associated with protection from Alzheimer's disease.
Bouzid H et al.
Nature Medicine, 2023
Cancer-driving mutations are enriched in genic regions intolerant to germline variation.
Vitsios D et al.
Science Advances, 2022
Genome-wide analyses of 200,453 individuals yield new insights into the causes and consequences of clonal hematopoiesis.
Kar SP et al.
Nature Genetics, 2022
Inherited causes of clonal haematopoiesis in 97,691 whole genomes.
Bick AG et al.
Nature, 2020
A splice site-sensing conformational switch in U2AF2 is modulated by U2AF1 and its recurrent myelodysplasia-associated mutation.
Warnasooriya C et al.
Nucleic Acids Research, 2020
The Augmented R-Loop Is a Unifying Mechanism for Myelodysplastic Syndromes Induced by High-Risk Splicing Factor Mutations.
Chen L et al.
Molecular Cell, 2018
An extended U2AF(65)-RNA-binding domain recognizes the 3' splice site signal.
Agrawal AA et al.
Nature Communications, 2016
Mechanisms for U2AF to define 3' splice sites and regulate alternative splicing in the human genome.
Shao C et al.
Nature Structural & Molecular Biology, 2014
Frequent pathway mutations of splicing machinery in myelodysplasia.
Yoshida K et al.
Nature, 2011