Pages that link to "Q36737860"

The following pages link to Modulation of LMNA splicing as a strategy to treat prelamin A diseases. (Q36737860):

Displaying 31 items.

• Metformin decreases progerin expression and alleviates pathological defects of Hutchinson-Gilford progeria syndrome cells. (Q33914338) (← links)
• Splice-switching antisense oligonucleotides as therapeutic drugs (Q37211004) (← links)
• Antisense-Based Progerin Downregulation in HGPS-Like Patients' Cells (Q37293792) (← links)
• Hutchinson-Gilford Progeria Syndrome: A premature aging disease caused by LMNA gene mutations. (Q38885070) (← links)
• Current insights into LMNA cardiomyopathies: Existing models and missing LINCs (Q39104972) (← links)
• Intermediate filament proteins of digestive organs: physiology and pathophysiology (Q39209502) (← links)
• Welcome to the splice age: antisense oligonucleotide-mediated exon skipping gains wider applicability (Q39617548) (← links)
• Recent Advances in Understanding and Managing Cardiomyopathy. (Q41528372) (← links)
• MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation. (Q41601030) (← links)
• Seeking a Cure for One of the Rarest Diseases: Progeria (Q42371479) (← links)
• Emerging candidate treatment strategies for Hutchinson-Gilford progeria syndrome (Q47414799) (← links)
• A Novel Generalized Lipodystrophy-Associated Progeroid Syndrome Due to Recurrent Heterozygous LMNA p.T10I Mutation. (Q51249757) (← links)
• Vascular Smooth Muscle-Specific Progerin Expression Accelerates Atherosclerosis and Death in a Mouse Model of Hutchinson-Gilford Progeria Syndrome. (Q51766620) (← links)
• Gene Editing and Gene-Based Therapeutics for Cardiomyopathies. (Q52662536) (← links)
• An overview of treatment strategies for Hutchinson-Gilford Progeria syndrome. (Q55004770) (← links)
• Upregulation of the aging related LMNA splice variant progerin in dilated cardiomyopathy. (Q55447827) (← links)
• Efficient exon skipping of SGCG mutations mediated by phosphorodiamidate morpholino oligomers. (Q55496176) (← links)
• The Pathogenesis and Therapies of Striated Muscle Laminopathies (Q58693707) (← links)
• Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome (Q58694537) (← links)
• Correction of a Splicing Mutation Affecting an Unverricht-Lundborg Disease Patient by Antisense Therapy (Q58749769) (← links)
• The Emerging Role of Lamin C as an Important Isoform in Mechanophenotype (Q59137488) (← links)
• Non-invasive monitoring of alternative splicing outcomes to identify candidate therapies for myotonic dystrophy type 1 (Q59790609) (← links)
• Nuclear Lamin Protein C Is Linked to Lineage-Specific, Whole-Cell Mechanical Properties (Q60104000) (← links)
• Hutchinson-Gilford Progeria Syndrome-Current Status and Prospects for Gene Therapy Treatment (Q64242806) (← links)
• Vascular smooth muscle cell loss underpins the accelerated atherosclerosis in Hutchinson-Gilford progeria syndrome (Q64268116) (← links)
• Lamins and Lamin-Associated Proteins in Gastrointestinal Health and Disease. (Q64881706) (← links)
• Metabolic Dysfunction in Hutchinson-Gilford Progeria Syndrome (Q89660120) (← links)
• Pharmacotherapy to gene editing: potential therapeutic approaches for Hutchinson-Gilford progeria syndrome (Q89669919) (← links)
• Permanently Farnesylated Prelamin A, Progeria, and Atherosclerosis (Q90253263) (← links)
• A genome-first approach to aggregating rare genetic variants in LMNA for association with electronic health record phenotypes (Q92432192) (← links)
• Antisense-mediated splice intervention to treat human disease: the odyssey continues (Q92527297) (← links)