Cloning and Sequencing of the Complete cDNA Encoding the Human Insulin Receptor Related Receptor

Hänze, Jörg; Berthold, A.; Klammt, J; Gallaher, B. W.; Siebler, Thomas; Kratzsch, Jürgen; Elmlinger, Martin W.; Kieß, Wieland

doi:10.1055/s-2007-978702

Cited by 11 publications

(2 citation statements)

References 9 publications

(22 reference statements)

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“…Moreover, down-regulation of IGF1R function in cancerous cells can promote apoptosis and inhibit transformation [Bahr and Groner, 2004], making IGF1R a promising target for the treatment of cancer [Baserga, 2005]. Mammals possess a third receptor of the Ins receptor family, the insulin receptor-related receptor, the function of which remains to be discovered [Shier and Watt, 1989; Hanze et al, 1999]. The human insulin receptor-related receptor (INSRR; OMIM 147671) shares 51% identity with IGF1R and 49% identity with INSR.…”

Section: Introductionmentioning

confidence: 99%

RILM: a web-based resource to aid comparative and functional analysis of the insulin and IGF-1 receptor family

Garza-Garcia¹,

Patel

Driscoll

2007

Hum. Mutat.

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Communicated by Bruce GottliebThe metazoan receptors for insulin (INSR), insulin-like growth factor 1 (IGF1R), and other insulin-like molecules are transmembrane tyrosine kinases involved in the regulation of cell size, cell proliferation, development, signaling of nutritional and environmental conditions, and aging. Historically, mutations in the human insulin receptor have been studied because such changes often lead to severe insulin resistance. More recently, amino acid sequence alterations in the insulin receptor-like receptors of Drosophila melanogaster and Caenorhabditis elegans, as well as in the mouse insulin receptor have been the focus of attention. These modifications can have profound effects on growth, body size, metabolism, and aging. To integrate the many findings on insulin/IGF1 receptor structure and function across species we have created ''Receptors for Insulin and Insulin-like Molecules'' (RILM), a curated computer-based resource that displays residue-by-residue information on sequence homology, three-dimensional structure, structure/function annotation, and documented mutations. The resource includes data obtained from sequence and structure analysis tools, primary database resources, and published reports. The information is integrated via a structure-based multiple sequence alignment of diverse members of the family. RILM was designed to provide easy access to multiple data types that could prove useful in the analysis of the effect of mutations on protein structure and ligand binding within this receptor family. RILM is available at www.biochem.ucl.ac.uk/RILM. Hum Mutat 28(7), [660][661][662][663][664][665][666][667][668] 2007.

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Section: Introductionmentioning

confidence: 99%

RILM: a web-based resource to aid comparative and functional analysis of the insulin and IGF-1 receptor family

Garza-Garcia¹,

Patel

Driscoll

2007

Hum. Mutat.

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“…They are highly homologous in terms of amino acid sequence and structure and are in the IR family [2,5,7,8]. Almost certainly, these receptors form chimeric receptor hybrids of IGF-IR (αIRβIR,αIG FIRβIGFIR), IR-IRR (αIRβIR,αIRRβIRR) and IGF-IR-IRR (αIGFIRβIGFIR,αIRRβIRR) tetramers that depend on specific expression levels for each receptor type [9].…”

Section: Introductionmentioning

confidence: 99%

Glucose concentration and AMP-dependent kinase activation regulate expression of insulin receptor family members in rat islets and INS-1E beta cells

et al. 2005

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Aims/hypothesis: Glucose and the peptide growth factors insulin, IGF-I and IGF-II strongly regulate beta cell mass. Furthermore, beta cell expression of IGF-I receptor (Igf1r) and insulin receptor (Insr) is mandatory for several steps of insulin secretion. Materials and methods: We hypothesised that glucose concentration might regulate expression of Igf1r, Insr and insulin receptor-related receptor (Insrr) in islets and beta cells. Moreover, since the ratio of ATP:ADP is the most important intracellular mechanism involved in insulin secretion, and since depletion of ATP leads to AMP accumulation, we evaluated the role of AMP-activated protein kinase (AMPK) in glucose-dependent receptor regulation. Results: In rat islets, high glucose exposure (25 mmol/l) increased gene expression of Igf1r, Insr and Insrr but also of the metabolic glycolysis gene liver-type pyruvate kinase (Pklr) compared with intermediate (6.2 mmol/l) or low glucose concentration (1.6 mmol/l) after 24 h. In rat INS-1E beta cells, only Pklr expression was suppressed by low glucose as in islets, while Insr and Insrr were suppressed by high and increased by low glucose levels. Igf1r expression was suppressed by both high-and low-glucose concentration. Activation of AMPK by 5-amino-imidazolecarboxamide riboside (AICAR, 0.5 mmol/l) suppressed Pklr expression, but strongly stimulated gene expression of Igf1r, Insr and Insrr. Protein expression of IR and IGF-IR reflected glucose and AICARregulated mRNA expression of both receptors in INS-1E cells. Conclusions/interpretation: We conclude that glucose directly interacts with islet and beta cell expression of growth factor receptors that are mandatory for both beta cell growth and insulin secretion. Stimulation of Igf1r and Insr gene expression by the AMPK-activator AICAR might indicate involvement of AMPK in the regulation of Igf1r, Insr and Insrr expression in beta cells.

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Receptor Tyrosine Kinases

Matthews¹,

Gerritsen²

2010

Targeting Protein Kinases for Cancer Therapy

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Cloning and Sequencing of the Complete cDNA Encoding the Human Insulin Receptor Related Receptor

Cited by 11 publications

References 9 publications

RILM: a web-based resource to aid comparative and functional analysis of the insulin and IGF-1 receptor family

RILM: a web-based resource to aid comparative and functional analysis of the insulin and IGF-1 receptor family

Glucose concentration and AMP-dependent kinase activation regulate expression of insulin receptor family members in rat islets and INS-1E beta cells

Receptor Tyrosine Kinases

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