Insulin receptor.

被引：0

作者：

Clauser, E

Auzan, C

Leconte, I

机构：

来源：

ANNALES D ENDOCRINOLOGIE | 1995年 / 56卷 / 05期

关键词：

insulin; receptor; protein; tyrosine-kinase; signalling;

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The cloning of the insulin receptor not only established the primary structure of this membrane-bound glycoprotein but also offered the material necessary for the study of the molecular functions of this tyrosine-kinase receptor using molecular biology tools. This short review will summarize the actual knowledge of the structure, the functions (molecular structure of the binding site, tyrosine-kinazse functions and role of autophosphorylation) and of the pathology of this receptor in extreme insulin resistances and type II diabetes.

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页码：515 / 521

页数：7

相关论文

共 25 条

[1] ON THE TERTIARY STRUCTURE OF THE EXTRACELLULAR DOMAINS OF THE EPIDERMAL GROWTH-FACTOR AND INSULIN-RECEPTORS [J].

BAJAJ, M ;

WATERFIELD, MD ;

SCHLESSINGER, J ;

TAYLOR, WR ;

BLUNDELL, T .

BIOCHIMICA ET BIOPHYSICA ACTA, 1987, 916 (02) :220-226

[2]

CANIVET B, TRAITE DIABETOLOGIE, P383

[3] CELLULAR ALTERATIONS IN LIVER, SKELETAL-MUSCLE, AND ADIPOSE-TISSUE RESPONSIBLE FOR INSULIN RESISTANCE IN OBESITY AND TYPE-II DIABETES [J].

CARO, JF ;

DOHM, LG ;

PORIES, WJ ;

SINHA, MK .

DIABETES-METABOLISM REVIEWS, 1989, 5 (08) :665-689

[4] NIDDM ASSOCIATED WITH MUTATION IN TYROSINE KINASE DOMAIN OF INSULIN-RECEPTOR GENE [J].

COCOZZA, S ;

PORCELLINI, A ;

RICCARDI, G ;

MONTICELLI, A ;

CONDORELLI, G ;

FERRARA, A ;

PIANESE, L ;

MIELE, C ;

CAPALDO, B ;

BEGUINOT, F ;

VARRONE, S .

DIABETES, 1992, 41 (04) :521-526

[5] THE HUMAN INSULIN-RECEPTOR CDNA - THE STRUCTURAL BASIS FOR HORMONE-ACTIVATED TRANSMEMBRANE SIGNALING [J].

EBINA, Y ;

ELLIS, L ;

JARNAGIN, K ;

EDERY, M ;

GRAF, L ;

CLAUSER, E ;

OU, JH ;

MASIARZ, F ;

KAN, YW ;

GOLDFINE, ID ;

ROTH, RA ;

RUTTER, WJ .

CELL, 1985, 40 (04) :747-758

[6] REPLACEMENT OF LYSINE RESIDUE 1030 IN THE PUTATIVE ATP-BINDING REGION OF THE INSULIN-RECEPTOR ABOLISHES INSULIN-STIMULATED AND ANTIBODY-STIMULATED GLUCOSE-UPTAKE AND RECEPTOR KINASE-ACTIVITY [J].

EBINA, Y ;

ARAKI, E ;

TAIRA, M ;

SHIMADA, F ;

MORI, M ;

CRAIK, CS ;

SIDDLE, K ;

PIERCE, SB ;

ROTH, RA ;

RUTTER, WJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (03) :704-708

[7] LINKAGE ANALYSIS OF INSULIN-RECEPTOR GENE IN FAMILIAL NIDDM [J].

ELBEIN, SC ;

SORENSEN, LK ;

TAYLOR, M .

DIABETES, 1992, 41 (05) :648-656

[8] REPLACEMENT OF INSULIN-RECEPTOR TYROSINE RESIDUES 1162 AND 1163 COMPROMISES INSULIN-STIMULATED KINASE-ACTIVITY AND UPTAKE OF 2-DEOXYGLUCOSE [J].

ELLIS, L ;

CLAUSER, E ;

MORGAN, DO ;

EDERY, M ;

ROTH, RA ;

RUTTER, WJ .

CELL, 1986, 45 (05) :721-732

[9] INSULIN ACTION, DIABETOGENES, AND THE CAUSE OF TYPE-II DIABETES [J].

KAHN, CR .

DIABETES, 1994, 43 (08) :1066-1084

[10]

LECONTE I, 1992, J BIOL CHEM, V267, P17415