The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Rad: a Member of the Ras Family Overexpressed in Muscle of Type II Diabetic Humans
Abstract
To identify the gene or genes associated with insulin resistance in Type II (non-insulin-dependent) diabetes mellitus, subtraction libraries were prepared from skeletal muscle of normal and diabetic humans and screened with subtracted probes. Only one clone out of 4000 was selectively overexpressed in Type II diabetic muscle as compared to muscle of non-diabetic or Type I diabetic individuals. This clone encoded a new 29-kilodalton member of the Ras-guanosine triphosphatase superfamily and was termed Rad (Ras associated with diabetes). Messenger ribonucleic acid of Rad was expressed primarily in skeletal and cardiac muscle and was increased an average of 8.6-fold in the muscle of Type II diabetics as compared to normal individuals.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“A few small GTPases containing substitutions at one or two of these positions have been found to maintain and exhibit GTPase activity in spite of the difference (37, 49).”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [49]
Citations
Cites
The GTPase superfamily: conserved structure and molecular mechanism
Bourne, H. R., Sanders, D. A., & McCormick, F. (1991) · Nature · doi:10.1038/349117a0 · Cited by 3,392
The Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDM
DeFronzo, R. A. (1988) · Diabetes · doi:10.2337/diab.37.6.667 · Cited by 2,456
Shulman, G. I., Rothman, D. L., Jue, T., Stein, P., DeFronzo, R. A., & Shulman, R. G. (1990) · New England Journal of Medicine · doi:10.1056/nejm199001253220403 · Cited by 1,248
Martin, B. C., Warram, J. H., Krolewski, A. S., Soeldner, J. S., Kahn, C. R., Martin, B. C., & Bergman, R. N. (1992) · The Lancet · doi:10.1016/0140-6736(92)92814-v · Cited by 1,158
Self-citationWarram, J. H., Martin, B. C., Krolewski, A. S., Soeldner, J. S., & Kahn, C. R. (1990) · Annals of Internal Medicine · doi:10.7326/0003-4819-113-12-909 · Cited by 1,038
Self-citationCaro, J. F., Sinha, M. K., Raju, S. M., Ittoop, O., Pories, W. J., Flickinger, E. G., Meelheim, D., & Dohm, G. L. (1987) · Journal of Clinical Investigation · doi:10.1172/jci112958 · Cited by 341
Research works printed but not linked: 52
- ALBRIGHT, C.F., CHARACTERIZATION OF A GUANINE-NUCLEOTIDE DISSOCIATION STIMULATOR FOR A RAS-RELATED GTPASE, EMBO JOURNAL 12: 339 (1993). · DOI
- BALDINI, G, CLONING OF A RAB3 ISOTYPE PREDOMINATELY EXPRESSED IN ADIPOCYTES, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 89: 5049 (1992).
- BALLINGER, S.W., MATERNALLY TRANSMITTED DIABETES AND DEAFNESS ASSOCIATED WITH A 10.4 KB MITOCHONDRIAL-DNA DELETION, NATURE GENETICS 1: 11 (1992). · DOI
- 10.1126/science.8391166 · DOI
- 10.1146/annurev.bi.56.070187.004023 · DOI · Paper page
- BARNETT, A.H., DIABETES IN IDENTICAL-TWINS - A STUDY OF 200 PAIRS, DIABETOLOGIA 20: 87 (1981). · DOI
- BECKNIELSEN, H, INSULIN RESISTANCE IN SKELETAL-MUSCLES IN PATIENTS WITH NIDDM, DIABETES CARE 15: 418 (1992). · DOI
- BELL, G.I., MOLECULAR DEFECTS IN DIABETES-MELLITUS, DIABETES 40: 413 (1991). · DOI
- BELL, G.I., GENE FOR NON-INSULIN-DEPENDENT DIABETES-MELLITUS (MATURITY-ONSET DIABETES OF THE YOUNG SUBTYPE) IS LINKED TO DNA POLYMORPHISM ON HUMAN CHROMOSOME-20Q, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 88: 1484 (1991).
- BOGARDUS, C, DISTRIBUTION OF INVIVO INSULIN ACTION IN PIMA-INDIANS AS MIXTURE OF 3 NORMAL-DISTRIBUTIONS, DIABETES 38: 1423 (1989). · DOI
- BURGERING, BMT, INSULIN STIMULATION OF GENE-EXPRESSION MEDIATED BY P21RAS ACTIVATION, EMBO JOURNAL 10: 1103 (1991). · DOI
- BURGERING, BMT, POSSIBLE INVOLVEMENT OF NORMAL P21 H-RAS IN THE INSULIN INSULINLIKE GROWTH FACTOR-I SIGNAL TRANSDUCTION PATHWAY, MOLECULAR AND CELLULAR BIOLOGY 9: 4312 (1989).
- CHUNG, D.L., A PEPTIDE FROM THE GAP-BINDING DOMAIN OF THE RAS-P21 PROTEIN AS WELL AS AZATYROSINE BLOCK RAS-INDUCED MATURATION OF XENOPUS-OOCYTES, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 181: 1378 (1991). · DOI
- CORMONT, M, INSULIN AND OKADAIC ACID INDUCE RAB4 REDISTRIBUTION IN ADIPOCYTES, JOURNAL OF BIOLOGICAL CHEMISTRY 268: 19491 (1993). · DOI
- COX, A.D., CURR OPIN CELL BIOL 4: 1008 (1992). · DOI · Paper page
- COX, N.J., LINKAGE STUDIES ON NIDDM AND THE INSULIN AND INSULIN-RECEPTOR GENES, DIABETES 38: 653 (1989). · DOI
- DESHPANDE, A.K., INSULIN INDUCTION OF XENOPUS-LAEVIS OOCYTE MATURATION IS INHIBITED BY MONOCLONAL-ANTIBODY AGAINST P21 RAS PROTEINS, MOLECULAR AND CELLULAR BIOLOGY 7: 1285 (1987).
- DRUGUID, J.R., PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 85: 5738 (1988).
- ELBEIN, S.C., MOLECULAR-GENETIC ANALYSIS AND ASSESSMENT OF INSULIN ACTION AND PANCREATIC BETA-CELL FUNCTION, DIABETES 37: 377 (1988). · DOI
- 10.1126/science.8484117 · DOI
- FLIER, J.S., DIABETES 41: 416 (1992). · DOI
- 10.1038/356162a0 · DOI
- FROGUEL, P, FAMILIAL HYPERGLYCEMIA DUE TO MUTATIONS IN GLUCOKINASE - DEFINITION OF A SUBTYPE OF DIABETES-MELLITUS, NEW ENGLAND JOURNAL OF MEDICINE 328: 697 (1993). · DOI
- 10.1126/science.2116664 · DOI
- HANCOCK, J.F., A CAAX OR A CAAL MOTIF AND A 2ND SIGNAL ARE SUFFICIENT FOR PLASMA-MEMBRANE TARGETING OF RAS PROTEINS, EMBO JOURNAL 10: 4033 (1991). · DOI
- 10.1016/0140-6736(92)91958-B · DOI
- KAELIN, W.G., EXPRESSION CLONING OF A CDNA-ENCODING A RETINOBLASTOMA-BINDING PROTEIN WITH E2F-LIKE PROPERTIES, CELL 70: 351 (1992). · DOI
- KLARLUND, J.K., ACTIVATION OF PROTEIN-KINASES BY INSULIN AND NONHYDROLYZABLE GTP ANALOGS IN PERMEABILIZED 3T3-L1 ADIPOCYTES, JOURNAL OF BIOLOGICAL CHEMISTRY 268: 7646 (1993). · DOI
- KNOWLER, W.C., DIABETES-MELLITUS IN THE PIMA-INDIANS - INCIDENCE, RISK-FACTORS AND PATHOGENESIS, DIABETES-METABOLISM REVIEWS 6: 1 (1990). · DOI · Paper page
- 10.1126/science.3554510 · DOI
- LILLIOJA, S, INVIVO INSULIN ACTION IS FAMILIAL CHARACTERISTIC IN NONDIABETIC PIMA-INDIANS, DIABETES 36: 1329 (1987). · DOI
- LU, K.H., RAS PROTEINS ARE ESSENTIAL AND SELECTIVE FOR THE ACTION OF INSULIN-LIKE GROWTH FACTOR-I LATE IN THE G1-PHASE OF THE CELL-CYCLE IN BALB/C MURINE FIBROBLASTS, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 89: 3889 (1992).
- MARTIN, B.C., FAMILIAL CLUSTERING OF INSULIN SENSITIVITY, DIABETES 41: 850 (1992). · DOI
- MCCLAIN, D.A., RESTRICTION-FRAGMENT LENGTH POLYMORPHISM IN INSULIN-RECEPTOR GENE AND INSULIN RESISTANCE IN NIDDM, DIABETES 37: 1071 (1988). · DOI
- MCCORMICK, F, SIGNAL TRANSDUCTION - HOW RECEPTORS TURN RAS ON, NATURE 363: 15 (1993). · DOI · Paper page
- MEDEMA, R.H., 2 DOMINANT INHIBITORY MUTANTS OF P21RAS INTERFERE WITH INSULIN-INDUCED GENE-EXPRESSION, MOLECULAR AND CELLULAR BIOLOGY 11: 5963 (1991).
- MEDEMA, R.H., RAS ACTIVATION BY INSULIN AND EPIDERMAL GROWTH-FACTOR THROUGH ENHANCED EXCHANGE OF GUANINE-NUCLEOTIDES ON P21RAS, MOLECULAR AND CELLULAR BIOLOGY 13: 155 (1993).
- MOLLER, D.E., BIOLOGIC ACTIVITIES OF NATURALLY-OCCURRING HUMAN INSULIN-RECEPTOR MUTATIONS - EVIDENCE THAT METABOLIC EFFECTS OF INSULIN CAN BE MEDIATED BY A KINASE-DEFICIENT INSULIN-RECEPTOR MUTANT, JOURNAL OF BIOLOGICAL CHEMISTRY 266: 10995 (1991). · DOI
- NEWMAN, B, CONCORDANCE FOR TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS IN MALE TWINS, DIABETOLOGIA 30: 763 (1987).
- OKAMOTO, T, REGULATION OF TRANSMEMBRANE SIGNAL TRANSDUCTION OF INSULIN-LIKE GROWTH FACTOR-II BY COMPETENCE TYPE GROWTH-FACTORS OR VIRAL RAS P21, JOURNAL OF BIOLOGICAL CHEMISTRY 266: 1085 (1991). · DOI
- OSTEROP, APRM, RELATION BETWEEN THE INSULIN-RECEPTOR NUMBER IN CELLS, AUTOPHOSPHORYLATION AND INSULIN-STIMULATED RAS-BULLET-GTP FORMATION, JOURNAL OF BIOLOGICAL CHEMISTRY 267: 14647 (1992). · DOI
- POLAKIS, P, STRUCTURAL REQUIREMENTS FOR THE INTERACTION OF P21RAS WITH GAP, EXCHANGE FACTORS, AND ITS BIOLOGICAL EFFECTOR TARGET, JOURNAL OF BIOLOGICAL CHEMISTRY 268: 9157 (1993). · DOI
- PORRAS, A, ACTIVATION OF RAS BY INSULIN IN 3T3-L1 CELLS DOES NOT INVOLVE GTPASE-ACTIVATING PROTEIN-PHOSPHORYLATION, JOURNAL OF BIOLOGICAL CHEMISTRY 267: 21124 (1992). · DOI
- RICH, S.S., MAPPING GENES IN DIABETES - GENETIC EPIDEMIOLOGIC PERSPECTIVE, DIABETES 39: 1315 (1990).
- SANDERS, D.A., A GUIDE TO LOW-MOLECULAR-WEIGHT GTPASES, CELL GROWTH & DIFFERENTIATION 1: 251 (1990).
- SCHUMACHER, M.C., MAJOR GENE EFFECT FOR INSULIN LEVELS IN FAMILIAL NIDDM PEDIGREES, DIABETES 41: 416 (1992). · DOI
- SCHWEINFEST, C. W., GENETIC ANALYSIS-BIOMOLECULAR ENGINEERING 7: 64 (1990).
- 10.1126/science.8316835 · DOI
- STEINER, D.F., LESSONS LEARNED FROM MOLECULAR-BIOLOGY OF INSULIN-GENE MUTATIONS, DIABETES CARE 13: 600 (1990). · DOI
- TAYLOR, S.I., GENETIC-BASIS OF ENDOCRINE DISEASE .1. MOLECULAR-GENETICS OF INSULIN RESISTANT DIABETES-MELLITUS, JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM 73: 1158 (1991). · DOI
- VALENCIA, A, THE RAS PROTEIN FAMILY - EVOLUTIONARY TREE AND ROLE OF CONSERVED AMINO-ACIDS, BIOCHEMISTRY 30: 4637 (1991). · DOI
- VANDEROUWELAND, M.W., NAT GENET 1: 368 (1992). · DOI
Cited by
Nonalcoholic Fatty Liver Disease
Angulo, P. (2002) · New England Journal of Medicine · doi:10.1056/nejmra011775 · Cited by 5,228
Glucose Transporters and Insulin Action — Implications for Insulin Resistance and Diabetes Mellitus
Shepherd, P. R., & Kahn, B. B. (1999) · New England Journal of Medicine · doi:10.1056/nejm199907223410406 · Cited by 1,295
Protein–protein interaction in insulin signaling and the molecular mechanisms of insulin resistance
Virkamäki, A., Ueki, K., & Kahn, C. R. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6609 · Cited by 854
Self-citationThe role of TNFα and TNF receptors in obesity and insulin resistance
Hotamisligil, G. S. (1999) · Journal of Internal Medicine · doi:10.1046/j.1365-2796.1999.00490.x · Cited by 780
Time- and exercise-dependent gene regulation in human skeletal muscle
Zambon, A. C., McDearmon, E. L., Salomonis, N., Vranizan, K. M., Johansen, K. L., Adey, D., Takahashi, J. S., Schambelan, M., & Conklin, B. R. (2003) · Genome Biology · doi:10.1186/gb-2003-4-10-r61 · Cited by 254
Metadata
- Authors
- Reynet, C., & Kahn, C. R.
- Affiliations
- Research Division, Joslin Diabetes Center, and Department of Medicine, Harvard Medical School, Boston, MA 02215.
- Venue
- Science
- Published
- 1993-11-26
- Volume
- 262
- Issue
- 5138
- Pages
- 1441-1444
- ISSN
- 0036-8075
- 1095-9203
- Cited by
- 254
- References
- 6
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Rad: a Member of the Ras Family Overexpressed in Muscle of Type II Diabetic Humans. https://app.cochat.ai/papers/10.1126/science.8248782
- The paper
- Reynet, C., & Kahn, C. R. (1993). Rad: a Member of the Ras Family Overexpressed in Muscle of Type II Diabetic Humans. Science. https://doi.org/10.1126/science.8248782