3.4.24.84 Acanthosis Nigricans http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20814950&form=6&db=m Early onset mandibuloacral dysplasia due to compound heterozygous mutations in ZMPSTE24. causal interaction,diagnostic usage,unassigned 4,2,0 3.4.24.84 Acro-Osteolysis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16278265&form=6&db=m A homozygous mutation in the lamin A/C gene associated with a novel syndrome of arthropathy, tendinous calcinosis, and progeroid features. causal interaction,unassigned 4,0 3.4.24.84 Acro-Osteolysis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20631028&form=6&db=m A novel syndrome of mandibular hypoplasia, deafness, and progeroid features associated with lipodystrophy, undescended testes, and male hypogonadism. causal interaction,unassigned 3,0 3.4.24.84 Acro-Osteolysis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20814950&form=6&db=m Early onset mandibuloacral dysplasia due to compound heterozygous mutations in ZMPSTE24. causal interaction,diagnostic usage,unassigned 4,2,0 3.4.24.84 Acro-Osteolysis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26602028&form=6&db=m A novel homozygous LMNA mutation (p.Met540Ile) causes mandibuloacral dysplasia type A. causal interaction,unassigned 3,0 3.4.24.84 Alopecia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18587406&form=6&db=m Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging. therapeutic application,unassigned 1,0 3.4.24.84 Atherosclerosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26724531&form=6&db=m LMNA mutations resulting in lipodystrophy and HIV protease inhibitors trigger vascular smooth muscle cell senescence and calcification: Role of ZMPSTE24 downregulation. causal interaction,unassigned 4,0 3.4.24.84 Carcinogenesis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27729169&form=6&db=m Mutational and expressional alterations of ZMPSTE24, DNA damage response-related gene, in gastric and colorectal cancers. causal interaction,diagnostic usage,ongoing research,unassigned 2,3,4,0 3.4.24.84 Carcinoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10373325&form=6&db=m Identification and chromosomal location of two human genes encoding enzymes potentially involved in proteolytic maturation of farnesylated proteins. ongoing research,unassigned 1,0 3.4.24.84 Cardiomyopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27120622&form=6&db=m A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.84 Cardiomyopathy, Dilated http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27120622&form=6&db=m A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.84 Colorectal Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27729169&form=6&db=m Mutational and expressional alterations of ZMPSTE24, DNA damage response-related gene, in gastric and colorectal cancers. causal interaction,diagnostic usage,ongoing research,unassigned 2,3,4,0 3.4.24.84 COVID-19 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34003736&form=6&db=m ZMPSTE24 Regulates SARS-CoV-2 Spike Protein-enhanced Expression of Endothelial PAI-1. causal interaction,ongoing research,unassigned 4,1,0 3.4.24.84 Cowpox http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28246125&form=6&db=m ZMPSTE24 defends against influenza and other pathogenic viruses. therapeutic application,unassigned 1,0 3.4.24.84 Cowpox http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28594571&form=6&db=m ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity. unassigned - 3.4.24.84 Dental Caries http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=24810274&form=6&db=m Genetic Association of MPPED2 and ACTN2 with Dental Caries. unassigned - 3.4.24.84 Genetic Diseases, Inborn http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26602028&form=6&db=m A novel homozygous LMNA mutation (p.Met540Ile) causes mandibuloacral dysplasia type A. causal interaction,unassigned 3,0 3.4.24.84 Glomerulosclerosis, Focal Segmental http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17152860&form=6&db=m Focal segmental glomerulosclerosis in patients with mandibuloacral dysplasia owing to ZMPSTE24 deficiency. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.84 Hearing Loss, Sensorineural http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20631028&form=6&db=m A novel syndrome of mandibular hypoplasia, deafness, and progeroid features associated with lipodystrophy, undescended testes, and male hypogonadism. causal interaction,unassigned 3,0 3.4.24.84 Heart Failure http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32872320&form=6&db=m ZMPSTE24 Is Associated with Elevated Inflammation and Progerin mRNA. diagnostic usage,ongoing research,unassigned 1,4,0 3.4.24.84 Infections http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28594571&form=6&db=m ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity. unassigned - 3.4.24.84 Influenza, Human http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28246125&form=6&db=m ZMPSTE24 defends against influenza and other pathogenic viruses. therapeutic application,unassigned 1,0 3.4.24.84 Influenza, Human http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28594571&form=6&db=m ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity. unassigned - 3.4.24.84 Joint Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16278265&form=6&db=m A homozygous mutation in the lamin A/C gene associated with a novel syndrome of arthropathy, tendinous calcinosis, and progeroid features. causal interaction,unassigned 4,0 3.4.24.84 Kidney Failure, Chronic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17152860&form=6&db=m Focal segmental glomerulosclerosis in patients with mandibuloacral dysplasia owing to ZMPSTE24 deficiency. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15317753&form=6&db=m Lamin A and ZMPSTE24 (FACE-1) defects cause nuclear disorganization and identify restrictive dermopathy as a lethal neonatal laminopathy. unassigned - 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15843403&form=6&db=m Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors. unassigned - 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16186497&form=6&db=m Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome. causal interaction,therapeutic application,unassigned 3,4,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16297189&form=6&db=m Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy. causal interaction,unassigned 3,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16364671&form=6&db=m Laminopathies: multisystem dystrophy syndromes. causal interaction,unassigned 3,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19014358&form=6&db=m Microcephalia with mandibular and dental dysplasia in adult Zmpste24-deficient mice. unassigned - 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19645629&form=6&db=m LMNA, ZMPSTE24, and LBR are not mutated in scleroderma. causal interaction,unassigned 1,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20074077&form=6&db=m HIV protease inhibitors inhibit FACE1/ZMPSTE24: a mechanism for acquired lipodystrophy in patients on highly active antiretroviral therapy? causal interaction,therapeutic application,unassigned 4,4,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27120622&form=6&db=m A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29484800&form=6&db=m Changes at the nuclear lamina alter binding of pioneer factor Foxa2 in aged liver. ongoing research,unassigned 1,0 3.4.24.84 Laminopathies http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33590450&form=6&db=m Lonafarnib: First Approval. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.84 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28246125&form=6&db=m ZMPSTE24 defends against influenza and other pathogenic viruses. therapeutic application,unassigned 1,0 3.4.24.84 Leukemia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28594571&form=6&db=m ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity. unassigned - 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17320032&form=6&db=m [Primary lipodystrophies] causal interaction,unassigned 4,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18230615&form=6&db=m A Potent HIV Protease Inhibitor, Darunavir, Does Not Inhibit ZMPSTE24 or Lead to an Accumulation of Farnesyl-prelamin A in Cells. causal interaction,therapeutic application,unassigned 4,3,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18587406&form=6&db=m Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging. therapeutic application,unassigned 1,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18639527&form=6&db=m HIV-protease inhibitors block the enzymatic activity of purified Ste24p. therapeutic application,unassigned 4,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20814950&form=6&db=m Early onset mandibuloacral dysplasia due to compound heterozygous mutations in ZMPSTE24. causal interaction,diagnostic usage,unassigned 4,2,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21828285&form=6&db=m Proteomic profiling of adipose tissue from Zmpste24-/- mice, a model of lipodystrophy and premature ageing, reveals major changes in mitochondrial function and vimentin processing. causal interaction,ongoing research,therapeutic application,unassigned 3,1,1,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21865368&form=6&db=m Lipodystrophies: Genetic and Acquired Body Fat Disorders. causal interaction,therapeutic application,unassigned 2,3,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22570643&form=6&db=m Hallermann-Streiff Syndrome: No Evidence for a Link to Laminopathies. causal interaction,therapeutic application,unassigned 3,1,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26602028&form=6&db=m A novel homozygous LMNA mutation (p.Met540Ile) causes mandibuloacral dysplasia type A. causal interaction,unassigned 3,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=26724531&form=6&db=m LMNA mutations resulting in lipodystrophy and HIV protease inhibitors trigger vascular smooth muscle cell senescence and calcification: Role of ZMPSTE24 downregulation. causal interaction,unassigned 4,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27410998&form=6&db=m Failure of ossification of the occipital bone in mandibuloacral dysplasia type B. causal interaction,ongoing research,unassigned 3,1,0 3.4.24.84 Lipodystrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27841971&form=6&db=m LMNA missense mutations causing familial partial lipodystrophy do not lead to an accumulation of prelamin A. unassigned - 3.4.24.84 Lipodystrophy, Congenital Generalized http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=25286833&form=6&db=m Mandibuloacral dysplasia type A-associated progeria caused by homozygous LMNA mutation in a family from Southern China. causal interaction,unassigned 3,0 3.4.24.84 Liver Cirrhosis, Biliary http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20522425&form=6&db=m LBR mutation and nuclear envelope defects in a patient affected with Reynolds syndrome. unassigned - 3.4.24.84 Lung Injury http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30158154&form=6&db=m Preventing loss of mechanosensation by the nuclear membranes of alveolar cells reduces lung injury in mice during mechanical ventilation. causal interaction,diagnostic usage,ongoing research,therapeutic application 4,3,4,4 3.4.24.84 Lymphoma http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=10373325&form=6&db=m Identification and chromosomal location of two human genes encoding enzymes potentially involved in proteolytic maturation of farnesylated proteins. ongoing research,unassigned 1,0 3.4.24.84 Metabolic Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27120622&form=6&db=m A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.84 Metabolic Syndrome http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=34003736&form=6&db=m ZMPSTE24 Regulates SARS-CoV-2 Spike Protein-enhanced Expression of Endothelial PAI-1. causal interaction,ongoing research,unassigned 4,1,0 3.4.24.84 Micrognathism http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20814950&form=6&db=m Early onset mandibuloacral dysplasia due to compound heterozygous mutations in ZMPSTE24. causal interaction,diagnostic usage,unassigned 4,2,0 3.4.24.84 Muscle Weakness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12235369&form=6&db=m Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. causal interaction,ongoing research,unassigned 4,2,0 3.4.24.84 Muscle Weakness http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21713376&form=6&db=m Skeletal muscle contractile function and neuromuscular performance in Zmpste24 (-/-) mice, a murine model of human progeria. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.84 Muscular Atrophy http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21713376&form=6&db=m Skeletal muscle contractile function and neuromuscular performance in Zmpste24 (-/-) mice, a murine model of human progeria. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.84 Muscular Diseases http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21267004&form=6&db=m Type B mandibuloacral dysplasia with congenital myopathy due to homozygous ZMPSTE24 missense mutation. causal interaction,unassigned 4,0 3.4.24.84 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19680556&form=6&db=m Genetic variation in healthy oldest-old. unassigned - 3.4.24.84 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23917225&form=6&db=m Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion. causal interaction,ongoing research,therapeutic application,unassigned 3,4,4,0 3.4.24.84 Neoplasms http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27729169&form=6&db=m Mutational and expressional alterations of ZMPSTE24, DNA damage response-related gene, in gastric and colorectal cancers. causal interaction,diagnostic usage,ongoing research,unassigned 2,3,4,0 3.4.24.84 Obesity, Abdominal http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27120622&form=6&db=m A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.84 Osteoporosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15984427&form=6&db=m Application of micro-CT assessment of 3-D bone microstructure in preclinical and clinical studies. causal interaction,ongoing research,therapeutic application,unassigned 3,1,1,0 3.4.24.84 Osteoporosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19587107&form=6&db=m Accelerated features of age-related bone loss in zmpste24 metalloproteinase-deficient mice. ongoing research,unassigned 3,0 3.4.24.84 Perinatal Death http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16671095&form=6&db=m A homozygous ZMPSTE24 null mutation in combination with a heterozygous mutation in the LMNA gene causes Hutchinson-Gilford progeria syndrome (HGPS): insights into the pathophysiology of HGPS. causal interaction,therapeutic application,unassigned 2,1,0 3.4.24.84 Premature Birth http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20814950&form=6&db=m Early onset mandibuloacral dysplasia due to compound heterozygous mutations in ZMPSTE24. causal interaction,diagnostic usage,unassigned 4,2,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15479179&form=6&db=m Hutchinson-Gilford progeria syndrome. therapeutic application,unassigned 2,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16671095&form=6&db=m A homozygous ZMPSTE24 null mutation in combination with a heterozygous mutation in the LMNA gene causes Hutchinson-Gilford progeria syndrome (HGPS): insights into the pathophysiology of HGPS. causal interaction,therapeutic application,unassigned 2,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19014358&form=6&db=m Microcephalia with mandibular and dental dysplasia in adult Zmpste24-deficient mice. unassigned - 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19351612&form=6&db=m Different prelamin A forms accumulate in human fibroblasts: a study in experimental models and progeria. unassigned - 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19680556&form=6&db=m Genetic variation in healthy oldest-old. unassigned - 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19851476&form=6&db=m Genomic Instability and DNA Damage Responses in Progeria Arising from Defective Maturation of Prelamin A. causal interaction,unassigned 4,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20458013&form=6&db=m Prelamin A acts to accelerate smooth muscle cell senescence and is a novel biomarker of human vascular aging. causal interaction,unassigned 4,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=20961378&form=6&db=m Nuclear envelope alterations generate an aging-like epigenetic pattern in mice deficient in Zmpste24 metalloprotease. causal interaction,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21549337&form=6&db=m Exome sequencing and functional analysis identifies BANF1 mutation as the cause of a hereditary progeroid syndrome. causal interaction,unassigned 2,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21713376&form=6&db=m Skeletal muscle contractile function and neuromuscular performance in Zmpste24 (-/-) mice, a murine model of human progeria. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21746928&form=6&db=m Histone H4 lysine 16 hypoacetylation is associated with defective DNA repair and premature senescence in Zmpste24-deficient mice. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22064465&form=6&db=m Micromanaging aging with miRNAs: New messages from the nuclear envelope. ongoing research,therapeutic application,unassigned 4,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22103512&form=6&db=m Cell autonomous and systemic factors in progeria development. causal interaction,unassigned 4,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22355414&form=6&db=m Requirements for Efficient Proteolytic Cleavage of Prelamin A by ZMPSTE24. therapeutic application,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22718200&form=6&db=m Human ZMPSTE24 disease mutations: residual proteolytic activity correlates with disease severity. causal interaction,unassigned 4,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=22933563&form=6&db=m Biogenesis of the Saccharomyces cerevisiae Pheromone a-Factor, from Yeast Mating to Human Disease. causal interaction,therapeutic application,unassigned 2,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23539603&form=6&db=m The structural basis of ZMPSTE24-dependent laminopathies. therapeutic application,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23695662&form=6&db=m Depleting the methyltransferase Suv39h1 improves DNA repair and extends lifespan in a progeria mouse model. ongoing research,therapeutic application,unassigned 2,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23804595&form=6&db=m Progeroid laminopathy with restrictive dermopathy-like features caused by an isodisomic LMNA mutation p.R435C. unassigned - 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=23917225&form=6&db=m Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion. causal interaction,ongoing research,therapeutic application,unassigned 3,4,4,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=27120622&form=6&db=m A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy. causal interaction,ongoing research,therapeutic application,unassigned 4,1,1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28990109&form=6&db=m miR?342?5p promotes Zmpste24?deficient mouse embryonic fibroblasts proliferation by suppressing GAS2. ongoing research,unassigned 3,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29567411&form=6&db=m Abnormal nuclear morphology is independent of longevity in a zmpste24-deficient fish model of Hutchinson-Gilford progeria syndrome (HGPS). therapeutic application,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29794150&form=6&db=m ZMPSTE24 missense mutations that cause progeroid diseases decrease prelamin A cleavage activity and/or protein stability. causal interaction,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30256865&form=6&db=m Different prelamin A forms accumulate in human fibroblasts: a study in experimental models and progeria. unassigned - 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30379953&form=6&db=m Next-Generation Sequencing and Quantitative Proteomics of Hutchinson-Gilford progeria syndrome-derived cells point to a role of nucleotide metabolism in premature aging. causal interaction,ongoing research,unassigned 1,3,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30625386&form=6&db=m A humanized yeast system to analyze cleavage of prelamin A by ZMPSTE24. therapeutic application,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31411525&form=6&db=m Dysfunction of iPSC-derived endothelial cells in human Hutchinson-Gilford progeria syndrome. ongoing research,unassigned 3,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33293369&form=6&db=m Site specificity determinants for prelamin A cleavage by the zinc metalloprotease ZMPSTE24. therapeutic application,unassigned 1,0 3.4.24.84 Progeria http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=33590450&form=6&db=m Lonafarnib: First Approval. causal interaction,therapeutic application,unassigned 2,4,0 3.4.24.84 Pulmonary Fibrosis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=30530916&form=6&db=m Accelerated aging induced by deficiency of Zmpste24 protects old mice to develop bleomycin-induced pulmonary fibrosis. causal interaction,unassigned 4,0 3.4.24.84 Scleroderma, Systemic http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=19645629&form=6&db=m LMNA, ZMPSTE24, and LBR are not mutated in scleroderma. causal interaction,unassigned 1,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=12235369&form=6&db=m Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. causal interaction,ongoing research,unassigned 4,2,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15608054&form=6&db=m Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice. causal interaction,unassigned 2,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=15984427&form=6&db=m Application of micro-CT assessment of 3-D bone microstructure in preclinical and clinical studies. causal interaction,ongoing research,therapeutic application,unassigned 3,1,1,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=16079796&form=6&db=m Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation. causal interaction,unassigned 4,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17152860&form=6&db=m Focal segmental glomerulosclerosis in patients with mandibuloacral dysplasia owing to ZMPSTE24 deficiency. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=17652517&form=6&db=m HIV protease inhibitors block the zinc metalloproteinase ZMPSTE24 and lead to an accumulation of prelamin A in cells. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18230615&form=6&db=m A Potent HIV Protease Inhibitor, Darunavir, Does Not Inhibit ZMPSTE24 or Lead to an Accumulation of Farnesyl-prelamin A in Cells. causal interaction,therapeutic application,unassigned 4,3,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18378773&form=6&db=m Nuclear envelope defects cause stem cell dysfunction in premature-aging mice. causal interaction,unassigned 4,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=18435794&form=6&db=m Severe mandibuloacral dysplasia caused by novel compound heterozygous ZMPSTE24 mutations in two Japanese siblings. causal interaction,unassigned 4,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21746928&form=6&db=m Histone H4 lysine 16 hypoacetylation is associated with defective DNA repair and premature senescence in Zmpste24-deficient mice. causal interaction,therapeutic application,unassigned 4,1,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=21828285&form=6&db=m Proteomic profiling of adipose tissue from Zmpste24-/- mice, a model of lipodystrophy and premature ageing, reveals major changes in mitochondrial function and vimentin processing. causal interaction,ongoing research,therapeutic application,unassigned 3,1,1,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28050601&form=6&db=m Progeroid syndrome patients with ZMPSTE24 deficiency could benefit when treated with rapamycin and dimethylsulfoxide. causal interaction,unassigned 4,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=29341437&form=6&db=m Phenotypic heterogeneity of ZMPSTE24 deficiency. causal interaction,unassigned 4,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=31941672&form=6&db=m Deficiency in ZMPSTE24 and resulting farnesyl-prelamin A accumulation only modestly affect mouse adipose tissue stores. causal interaction,unassigned 3,0 3.4.24.84 ste24 endopeptidase deficiency http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=32910507&form=6&db=m Targeting RAS-converting enzyme 1 overcomes senescence and improves progeria-like phenotypes of ZMPSTE24 deficiency. causal interaction,therapeutic application,unassigned 4,2,0 3.4.24.84 Vaccinia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28246125&form=6&db=m ZMPSTE24 defends against influenza and other pathogenic viruses. therapeutic application,unassigned 1,0 3.4.24.84 Vaccinia http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28594571&form=6&db=m ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity. unassigned - 3.4.24.84 Vesicular Stomatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28246125&form=6&db=m ZMPSTE24 defends against influenza and other pathogenic viruses. therapeutic application,unassigned 1,0 3.4.24.84 Vesicular Stomatitis http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=28594571&form=6&db=m ZMPSTE24 Is Downstream Effector of Interferon-Induced Transmembrane Antiviral Activity. unassigned -