INSULIN-RECEPTOR TYROSINE KINASE STRUCTURE AND FUNCTION

[1] BACKER JM, 1990, J BIOL CHEM, V265, P16450

[2] BOULTON TG, 1990, J BIOL CHEM, V265, P2713

[3] CHEN WJ, 1990, J BIOL CHEM, V265, P3116

[4] CHOU CK, 1987, J BIOL CHEM, V262, P1842

[5] COBB MH, 1989, J BIOL CHEM, V264, P18701

[6] REPLACEMENT OF INSULIN-RECEPTOR TYROSINE RESIDUE-1162 AND RESIDUE-1163 DOES NOT ALTER THE MITOGENIC EFFECT OF THE HORMONE [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (21) : 8032 - 8036

[7] THE HUMAN INSULIN-RECEPTOR CDNA - THE STRUCTURAL BASIS FOR HORMONE-ACTIVATED TRANSMEMBRANE SIGNALING [J]. CELL, 1985, 40 (04) : 747 - 758

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

[9] A MEMBRANE-ANCHORED CYTOPLASMIC DOMAIN OF THE HUMAN INSULIN-RECEPTOR MEDIATES A CONSTITUTIVELY ELEVATED INSULIN-INDEPENDENT UPTAKE OF 2-DEOXYGLUCOSE [J]. MOLECULAR ENDOCRINOLOGY, 1987, 1 (01) : 15 - 24

[10] REPLACEMENT OF INSULIN-RECEPTOR TYROSINE RESIDUES 1162 AND 1163 COMPROMISES INSULIN-STIMULATED KINASE-ACTIVITY AND UPTAKE OF 2-DEOXYGLUCOSE [J]. CELL, 1986, 45 (05) : 721 - 732

[1] BACKER JM, 1990, J BIOL CHEM, V265, P16450

[2] BOULTON TG, 1990, J BIOL CHEM, V265, P2713

[3] CHEN WJ, 1990, J BIOL CHEM, V265, P3116

[4] CHOU CK, 1987, J BIOL CHEM, V262, P1842

[5] COBB MH, 1989, J BIOL CHEM, V264, P18701

[6] REPLACEMENT OF INSULIN-RECEPTOR TYROSINE RESIDUE-1162 AND RESIDUE-1163 DOES NOT ALTER THE MITOGENIC EFFECT OF THE HORMONE [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (21) : 8032 - 8036

[7] THE HUMAN INSULIN-RECEPTOR CDNA - THE STRUCTURAL BASIS FOR HORMONE-ACTIVATED TRANSMEMBRANE SIGNALING [J]. CELL, 1985, 40 (04) : 747 - 758

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

[9] A MEMBRANE-ANCHORED CYTOPLASMIC DOMAIN OF THE HUMAN INSULIN-RECEPTOR MEDIATES A CONSTITUTIVELY ELEVATED INSULIN-INDEPENDENT UPTAKE OF 2-DEOXYGLUCOSE [J]. MOLECULAR ENDOCRINOLOGY, 1987, 1 (01) : 15 - 24

[10] REPLACEMENT OF INSULIN-RECEPTOR TYROSINE RESIDUES 1162 AND 1163 COMPROMISES INSULIN-STIMULATED KINASE-ACTIVITY AND UPTAKE OF 2-DEOXYGLUCOSE [J]. CELL, 1986, 45 (05) : 721 - 732