CELA2A mutations predispose to early-onset atherosclerosis and metabolic syndrome and affect plasma insulin and platelet activation

[1]  P. O’Reilly,et al.  Correction: Corrigendum: Genome-wide association analysis identifies novel blood pressure loci and offers biological insights into cardiovascular risk , 2017, Nature Genetics.

[2]  Andrew D. Johnson,et al.  Novel Blood Pressure Locus and Gene Discovery Using Genome-Wide Association Study and Expression Data Sets From Blood and the Kidney , 2017, Hypertension.

[3]  R. Mains,et al.  Brain Region and Isoform-Specific Phosphorylation Alters Kalirin SH2 Domain Interaction Sites and Calpain Sensitivity. , 2017, ACS chemical neuroscience.

[4]  N. Risch,et al.  Genome-wide association analyses using electronic health records identify new loci influencing blood pressure variation , 2016, Nature Genetics.

[5]  A. Szabó,et al.  Complex Formation of Human Proelastases with Procarboxypeptidases A1 and A2* , 2016, The Journal of Biological Chemistry.

[6]  Yu Jin,et al.  Inducing mitophagy in diabetic platelets protects against severe oxidative stress , 2016, EMBO molecular medicine.

[7]  Y. Hong,et al.  Associations of Sarcopenia and Sarcopenic Obesity With Metabolic Syndrome Considering Both Muscle Mass and Muscle Strength , 2015, Journal of preventive medicine and public health = Yebang Uihakhoe chi.

[8]  R. Colbran,et al.  Quantitative proteomics analysis of CaMKII phosphorylation and the CaMKII interactome in the mouse forebrain. , 2015, ACS chemical neuroscience.

[9]  R. Malekzadeh,et al.  A form of the metabolic syndrome associated with mutations in DYRK1B. , 2014, The New England journal of medicine.

[10]  G. Go,et al.  The combined hyperlipidemia caused by impaired Wnt-LRP6 signaling is reversed by Wnt3a rescue. , 2014, Cell metabolism.

[11]  C. Östenson,et al.  The Type 2 Diabetes–Associated Gene Ide Is Required for Insulin Secretion and Suppression of α-Synuclein Levels in β-Cells , 2013, Diabetes.

[12]  J. Holst,et al.  Secretion of glucagon-like peptide-1 in patients with type 2 diabetes mellitus: systematic review and meta-analyses of clinical studies , 2013, Diabetologia.

[13]  N. Stefan,et al.  Impairment of GLP1‐induced insulin secretion: role of genetic background, insulin resistance and hyperglycaemia , 2012, Diabetes, obesity & metabolism.

[14]  J. Olefsky,et al.  Neutrophils mediate insulin resistance in high fat diet fed mice via secreted elastase , 2012, Nature Medicine.

[15]  A. Clark,et al.  Recent Explosive Human Population Growth Has Resulted in an Excess of Rare Genetic Variants , 2012, Science.

[16]  Dennis C. Sgroi,et al.  Gene Expression Profiles of Beta-Cell Enriched Tissue Obtained by Laser Capture Microdissection from Subjects with Type 2 Diabetes , 2010, PloS one.

[17]  Deng-Chyang Wu,et al.  P-selectin-dependent platelet aggregation and apoptosis may explain the decrease in platelet count during Helicobacter pylori infection. , 2010, Blood.

[18]  P. Bork,et al.  A method and server for predicting damaging missense mutations , 2010, Nature Methods.

[19]  G. Lowe,et al.  Relative Value of Inflammatory, Hemostatic, and Rheological Factors for Incident Myocardial Infarction and Stroke: The Edinburgh Artery Study , 2007, Circulation.

[20]  Jayaram Radhakrishnan,et al.  LRP6 Mutation in a Family with Early Coronary Disease and Metabolic Risk Factors , 2007, Science.

[21]  E. Szepessy,et al.  Inactivity of Recombinant ELA2B Provides a New Example of Evolutionary Elastase Silencing in Humans , 2006, Pancreatology.

[22]  W. Catterall,et al.  Sites of proteolytic processing and noncovalent association of the distal C-terminal domain of CaV1.1 channels in skeletal muscle. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[23]  Nathan D. Wong,et al.  Impact of the Metabolic Syndrome on Mortality From Coronary Heart Disease, Cardiovascular Disease, and All Causes in United States Adults , 2004, Circulation.

[24]  Guohong Liu,et al.  Cav1.3 is preferentially coupled to glucose-induced [Ca2+]i oscillations in the pancreatic beta cell line INS-1. , 2004, Molecular pharmacology.

[25]  J. Weissenbach,et al.  Mutations in PCSK9 cause autosomal dominant hypercholesterolemia , 2003, Nature Genetics.

[26]  Matthew P. Frosch,et al.  Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[27]  C. Bogardus,et al.  Microarray profiling of skeletal muscle tissues from equally obese, non-diabetic insulin-sensitive and insulin-resistant Pima Indians , 2002, Diabetologia.

[28]  R. Wu,et al.  The anti-inflammatory compound lisofylline prevents Type I diabetes in non-obese diabetic mice , 2002, Diabetologia.

[29]  P. Touboul,et al.  Serum Elastase Activity, Serum Elastase Inhibitors, and Occurrence of Carotid Atherosclerotic Plaques: The Etude sur le Vieillissement Artériel (EVA) Study , 2002, Circulation.

[30]  Y. Kido,et al.  CEACAM1 regulates insulin clearance in liver , 2002, Nature Genetics.

[31]  M. Bünemann,et al.  C-terminal Fragments of the α1C(CaV1.2) Subunit Associate with and Regulate L-type Calcium Channels Containing C-terminal-truncated α1CSubunits* , 2001, The Journal of Biological Chemistry.

[32]  W. Kohrt,et al.  Effect of aging. , 2000, Nutrition reviews.

[33]  Alan D. Lopez,et al.  Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study , 1997, The Lancet.

[34]  C. Daly,et al.  Post-Transcriptional Regulation of Synaptic Vesicle Protein Expression and the Developmental Control of Synaptic Vesicle Formation , 1997, The Journal of Neuroscience.

[35]  M. Horie,et al.  Increased calcium-channel currents of pancreatic beta cells in neonatally streptozocin-induced diabetic rats. , 1994, Metabolism: clinical and experimental.

[36]  P. Frey,et al.  A low-barrier hydrogen bond in the catalytic triad of serine proteases. , 1994, Science.

[37]  L. Berkman,et al.  Genetic susceptibility to death from coronary heart disease in a study of twins. , 1994, The New England journal of medicine.

[38]  M. Jacob,et al.  Cell‐Matrix Interactions in the Genesis of Arteriosclerosis and Atheroma , 1992, Annals of the New York Academy of Sciences.

[39]  A. Frelinger,et al.  Activation of the fibrinogen receptor on human platelets exposed to alpha chymotrypsin. Relationship with a major proteolytic cleavage at the carboxyterminus of the membrane glycoprotein IIb heavy chain. , 1991, European journal of biochemistry.

[40]  A. Mitra,et al.  Degradation of Insulin by Trypsin and Alpha-Chymotrypsin , 1991, Pharmaceutical Research.

[41]  J. Powers,et al.  Irreversible inhibition of serine proteases by peptide derivatives of (alpha-aminoalkyl)phosphonate diphenyl esters. , 1991, Biochemistry.

[42]  R M Stroud,et al.  The three-dimensional structure of Asn102 mutant of trypsin: role of Asp102 in serine protease catalysis. , 1988, Science.

[43]  J. Hoxie,et al.  Changes in the platelet membrane glycoprotein IIb.IIIa complex during platelet activation. , 1985, The Journal of biological chemistry.

[44]  C. Largman,et al.  Purification and characterization of two human pancreatic elastases. , 1976, Biochemistry.

[45]  A. Fersht,et al.  The charge relay system in chymotrypsin and chymotrypsinogen. , 1973, Journal of molecular biology.

[46]  D. Selkoe,et al.  Insulin-degrading enzyme regulates the levels of insulin, amyloid beta-protein, and the beta-amyloid precursor protein intracellular domain in vivo. , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[47]  Alan D. Lopez,et al.  The Global Burden of Disease Study , 2003 .

[48]  M. Bunemann,et al.  C-terminal fragments of the alpha 1C (CaV1.2) subunit associate with and regulate L-type calcium channels containing C-terminal-truncated alpha 1C subunits. , 2001, The Journal of biological chemistry.

[49]  T. Iwamoto,et al.  Anti-atherosclerotic action of elastase--with special reference to its effect on elastic fibres. , 1983, Age and ageing.