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Article ; Online: Correction to: Cell-autonomous programming of rat adipose tissue insulin signalling proteins by maternal nutrition.

Martin-Gronert, Malgorzata S / Fernandez-Twinn, Denise S / Bushell, Martin / Siddle, Kenneth / Ozanne, Susan E

2023 Volume 67, Issue 1, Page(s) 216–217

Language	English
Publishing date	2023-11-06
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-023-06036-w
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Article ; Online: Molecular basis of signaling specificity of insulin and IGF receptors: neglected corners and recent advances.

Siddle, Kenneth

Frontiers in endocrinology

2012 Volume 3, Page(s) 34

Abstract: Insulin and insulin-like growth factor (IGF) receptors utilize common phosphoinositide 3-kinase/Akt and Ras/extracellular signal-regulated kinase signaling pathways to mediate a broad spectrum of "metabolic" and "mitogenic" responses. Specificity of ... ...

Abstract	Insulin and insulin-like growth factor (IGF) receptors utilize common phosphoinositide 3-kinase/Akt and Ras/extracellular signal-regulated kinase signaling pathways to mediate a broad spectrum of "metabolic" and "mitogenic" responses. Specificity of insulin and IGF action in vivo must in part reflect expression of receptors and responsive pathways in different tissues but it is widely assumed that it is also determined by the ligand binding and signaling mechanisms of the receptors. This review focuses on receptor-proximal events in insulin/IGF signaling and examines their contribution to specificity of downstream responses. Insulin and IGF receptors may differ subtly in the efficiency with which they recruit their major substrates (IRS-1 and IRS-2 and Shc) and this could influence effectiveness of signaling to "metabolic" and "mitogenic" responses. Other substrates (Grb2-associated binder, downstream of kinases, SH2Bs, Crk), scaffolds (RACK1, β-arrestins, cytohesins), and pathways (non-receptor tyrosine kinases, phosphoinositide kinases, reactive oxygen species) have been less widely studied. Some of these components appear to be specifically involved in "metabolic" or "mitogenic" signaling but it has not been shown that this reflects receptor-preferential interaction. Very few receptor-specific interactions have been characterized, and their roles in signaling are unclear. Signaling specificity might also be imparted by differences in intracellular trafficking or feedback regulation of receptors, but few studies have directly addressed this possibility. Although published data are not wholly conclusive, no evidence has yet emerged for signaling mechanisms that are specifically engaged by insulin receptors but not IGF receptors or vice versa, and there is only limited evidence for differential activation of signaling mechanisms that are common to both receptors. Cellular context, rather than intrinsic receptor activity, therefore appears to be the major determinant of whether responses to insulin and IGFs are perceived as "metabolic" or "mitogenic."
Language	English
Publishing date	2012-02-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392 ; 1664-2392
ISSN (online)	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2012.00034
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Article ; Online: Signalling by insulin and IGF receptors: supporting acts and new players.

Siddle, Kenneth

Journal of molecular endocrinology

2011 Volume 47, Issue 1, Page(s) R1–10

Abstract: The signalling pathways utilised by insulin receptor (IR) and IGF receptor to transduce their diverse effects on cellular metabolism, growth and survival are well established in broad outline, but many details remain to be elucidated. Tyrosine ... ...

Abstract	The signalling pathways utilised by insulin receptor (IR) and IGF receptor to transduce their diverse effects on cellular metabolism, growth and survival are well established in broad outline, but many details remain to be elucidated. Tyrosine phosphorylation of IR substrates and Shc initiates signalling via canonical phosphoinositide 3-kinase/Akt and Ras/MAP kinase pathways, which together mediate many of the actions of insulin and IGFs. However, a variety of additional substrates and scaffolds have been described that may play roles in modulating the canonical pathways or in specific biological responses. This review will focus on recent studies that have extended our understanding of insulin/IGF signalling pathways, and the elements that may contribute to specificity.
MeSH term(s)	Animals ; Glucose/metabolism ; Humans ; Insulin/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Protein Conformation ; Protein Transport ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins p21(ras)/metabolism ; Receptor, Insulin/chemistry ; Receptor, Insulin/metabolism ; Receptors, Somatomedin/metabolism ; Signal Transduction
Chemical Substances	Insulin ; Intracellular Signaling Peptides and Proteins ; Receptors, Somatomedin ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Receptor, Insulin (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2011-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1530/JME-11-0022
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Article ; Online: Correction to 'The human insulin receptor mRNA contains a functional internal ribosome entry segment'.

Spriggs, Keith A / Cobbold, Laura C / Ridley, Simon H / Coldwell, Mark / Bottley, Andrew / Bushell, Martin / Willis, Anne E / Siddle, Kenneth

Nucleic acids research

2022 Volume 50, Issue 3, Page(s) 1796–1798

Language	English
Publishing date	2022-01-31
Publishing country	England
Document type	Published Erratum
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkac063
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Book: Rural change in tropical Africa

Siddle, David / Swindell, Kenneth

from colonies to nation-states

(The Institute of British Geographers special publications series ; 23)

1990

Author's details	David Siddle and Kenneth Swindell
Series title	The Institute of British Geographers special publications series ; 23 Special publication / Institute of British Geographers
Collection	Special publication / Institute of British Geographers
Keywords	Subsaharisches Afrika ; Ländliche Entwicklung ; Entkolonialisierung
Subject	Dekolonialisierung ; Kolonialreich ; Dekolonisation ; Dekolonisierung ; Kolonialvolk ; Decolonisation ; Decolonization ; Integrierte ländliche Entwicklung ; Ländlicher Raum ; Ländliche Regionalentwicklung
Language	English
Size	221 S. : graph. Darst., Kt.
Publisher	Blackwell
Publishing place	Oxford u.a.
Publishing country	Great Britain
Document type	Book
HBZ-ID	HT003753374
ISBN	0-631-15855-3 ; 978-0-631-15855-4
Database	Catalogue ZB MED Nutrition, Environment, Agriculture

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Shelf mark	Loan status	Location
914/36	available for loan (reading room)	Freihandmagazin (U1)

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Article ; Online: Evaluation of anti-insulin receptor antibodies as potential novel therapies for human insulin receptoropathy using cell culture models.

Brierley, Gemma V / Siddle, Kenneth / Semple, Robert K

Diabetologia

2018 Volume 61, Issue 7, Page(s) 1662–1675

Abstract: Aims/hypothesis: Bi-allelic loss-of-function mutations in the INSR gene (encoding the insulin receptor [INSR]) commonly cause extreme insulin resistance and early mortality. Therapeutic options are limited, but anti-INSR antibodies have been shown to ... ...

Abstract	Aims/hypothesis: Bi-allelic loss-of-function mutations in the INSR gene (encoding the insulin receptor [INSR]) commonly cause extreme insulin resistance and early mortality. Therapeutic options are limited, but anti-INSR antibodies have been shown to activate two mutant receptors, S323L and F382V. This study evaluates four well-characterised murine anti-INSR monoclonal antibodies recognising distinct epitopes (83-7, 83-14, 18-44, 18-146) as surrogate agonists for potential targeted treatment of severe insulin resistance arising from insulin receptoropathies. Methods: Ten naturally occurring mutant human INSRs with defects affecting different aspects of receptor function were modelled and assessed for response to insulin and anti-INSR antibodies. A novel 3T3-L1 adipocyte model of insulin receptoropathy was generated, permitting conditional knockdown of endogenous mouse Insr by lentiviral expression of species-specific short hairpin (sh)RNAs with simultaneous expression of human mutant INSR transgenes. Results: All expressed mutant INSR bound to all antibodies tested. Eight mutants showed antibody-induced autophosphorylation, while co-treatment with antibody and insulin increased maximal phosphorylation compared with insulin alone. After knockdown of mouse Insr and expression of mutant INSR in 3T3-L1 adipocytes, two antibodies (83-7 and 83-14) activated signalling via protein kinase B (Akt) preferentially over signalling via extracellular signal-regulated kinase 1/2 (ERK1/2) for seven mutants. These antibodies stimulated glucose uptake via P193L, S323L, F382V and D707A mutant INSRs, with antibody response greater than insulin response for D707A. Conclusions/interpretation: Anti-INSR monoclonal antibodies can activate selected naturally occurring mutant human insulin receptors, bringing closer the prospect of novel therapy for severe insulin resistance caused by recessive mutations.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/drug effects ; Adipocytes/immunology ; Adipocytes/metabolism ; Animals ; Antibodies/pharmacology ; Antigens, CD/genetics ; Antigens, CD/immunology ; Antigens, CD/metabolism ; CHO Cells ; Cricetulus ; Glucose/metabolism ; Humans ; Hypoglycemic Agents/pharmacology ; Insulin/pharmacology ; Insulin Resistance/genetics ; Mice ; Mutation ; Phosphorylation ; Receptor, Insulin/agonists ; Receptor, Insulin/genetics ; Receptor, Insulin/immunology ; Receptor, Insulin/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antibodies ; Antigens, CD ; Hypoglycemic Agents ; Insulin ; INSR protein, human (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-04-27
Publishing country	Germany
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-018-4606-2
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Article ; Online: Anti-Insulin Receptor Antibodies Improve Hyperglycemia in a Mouse Model of Human Insulin Receptoropathy.

Brierley, Gemma V / Webber, Hannah / Rasijeff, Eerika / Grocott, Sarah / Siddle, Kenneth / Semple, Robert K

Diabetes

2020 Volume 69, Issue 11, Page(s) 2481–2489

Abstract: Loss-of-function mutations in both alleles of the human insulin receptor gene (INSR) cause extreme insulin resistance (IR) and usually death in childhood, with few effective therapeutic options. Bivalent antireceptor antibodies can elicit insulin-like ... ...

Abstract	Loss-of-function mutations in both alleles of the human insulin receptor gene (INSR) cause extreme insulin resistance (IR) and usually death in childhood, with few effective therapeutic options. Bivalent antireceptor antibodies can elicit insulin-like signaling by mutant INSR in cultured cells, but whether this translates into meaningful metabolic benefits in vivo, wherein the dynamics of insulin signaling and receptor recycling are more complex, is unknown. To address this, we adopted a strategy to model human insulin receptoropathy in mice, using
MeSH term(s)	Animals ; Antibodies ; Blood Glucose ; Disease Models, Animal ; Gene Expression Regulation ; Hyperglycemia/therapy ; Insulin/immunology ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Random Allocation ; Receptor, Insulin/genetics ; Receptor, Insulin/immunology ; Receptor, Insulin/metabolism
Chemical Substances	Antibodies ; Blood Glucose ; Insulin ; RNA, Messenger ; Receptor, Insulin (EC 2.7.10.1)
Language	English
Publishing date	2020-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db20-0345
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Article ; Online: Molecular basis of signalling specificity of insulin and IGF receptors

KennethSiddle

Frontiers in Endocrinology, Vol

neglected corners and new advances

2012 Volume 3

Abstract: Insulin and IGF receptors utilise common PI3K/Akt and Ras/ERK signalling pathways to mediate a broad spectrum of ‘metabolic’ and ‘mitogenic’ responses. Specificity of insulin and IGF action in vivo must in part reflect expression of receptors and ... ...

Abstract	Insulin and IGF receptors utilise common PI3K/Akt and Ras/ERK signalling pathways to mediate a broad spectrum of ‘metabolic’ and ‘mitogenic’ responses. Specificity of insulin and IGF action in vivo must in part reflect expression of receptors and responsive pathways in different tissues but it is widely assumed that it is also determined by the ligand binding and signalling mechanisms of the receptors. This review focuses on receptor-proximal events in insulin/IGF signalling and examines their contribution to specificity of downstream responses. Insulin and IGF receptors may differ subtly in the efficiency with which they recruit their major substrates (IRS-1 and -2 and Shc) and this could influence effectiveness of signalling to ‘metabolic’ and ‘mitogenic’ responses. Other substrates (Gabs, DOKs, SH2Bs, Crk), scaffolds (RACK1, β-arrestins, cytohesins) and pathways (non-receptor tyrosine kinases, phosphoinositide kinases, reactive oxygen species) have been less widely studied. Some of these components appear to be specifically involved in ‘metabolic’ or ‘mitogenic’ signalling but it has not been shown that this reflects receptor-preferential interaction. Very few receptor-specific interactions have been characterised, and their roles in signalling are unclear. Signalling specificity might also be imparted by differences in intracellular trafficking or feedback regulation of receptors, but few studies have directly addressed this possibility. Although published data are not wholly conclusive, no evidence has yet emerged for signalling mechanisms that are specifically engaged by insulin receptors but not IGF receptors or vice versa, and there is only limited evidence for differential activation of signalling mechanisms that are common to both receptors. Cellular context, rather than intrinsic receptor activity, therefore appears to be the major determinant of whether responses to insulin and IGFs are perceived as ‘metabolic’ or ‘mitogenic’.
Keywords	signalling ; specificity ; Scaffold ; adaptor ; IGF receptor ; Insulin receptor ; substrate ; Tyrosine Kinase ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R
Subject code	570
Language	English
Publishing date	2012-02-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
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Article ; Online: Two isoforms of the mRNA binding protein IGF2BP2 are generated by alternative translational initiation.

Le, Hang T T / Sorrell, Alice M / Siddle, Kenneth

PloS one

2012 Volume 7, Issue 3, Page(s) e33140

Abstract: IGF2BP2 is a member of a family of mRNA binding proteins that, collectively, have been shown to bind to several different mRNAs in mammalian cells, including one of the mRNAs encoding insulin-like growth factor-2. Polymorphisms in the Igf2bp2 gene are ... ...

Abstract	IGF2BP2 is a member of a family of mRNA binding proteins that, collectively, have been shown to bind to several different mRNAs in mammalian cells, including one of the mRNAs encoding insulin-like growth factor-2. Polymorphisms in the Igf2bp2 gene are associated with risk of developing type 2 diabetes, but detailed functional characterisation of IGF2BP2 protein is lacking. By immunoblotting with C-terminally reactive antibodies we identified a novel IGF2BP2 isoform with a molecular weight of 58 kDa in both human and rodents, that is expressed at somewhat lower levels than the full-length 65 kDa protein. We demonstrated by mutagenesis that this isoform is generated by alternative translation initiation at the internal Met69. It lacks a conserved N-terminal RNA Recognition Motif (RRM) and would be predicted to differ functionally from the canonical full length isoform. We further investigated IGF2BP2 mRNA transcripts by amplification of cDNA using 5'-RACE. We identified multiple transcription start sites of the human, mouse and rat Igf2bp2 genes in a highly conserved region only 50-90 nts upstream of the major translation start site, ruling out the existence of N-terminally extended isoforms. We conclude that structural heterogeneity of IGF2BP2 protein should be taken into account when considering cellular function.
MeSH term(s)	Amino Acid Sequence ; Animals ; Blotting, Western ; DNA, Complementary/genetics ; Humans ; Mice ; Molecular Sequence Data ; Mutagenesis ; Peptide Chain Initiation, Translational/genetics ; Peptide Chain Initiation, Translational/physiology ; Protein Isoforms/genetics ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Rats ; Sequence Analysis, DNA ; Species Specificity ; Transcription Initiation Site
Chemical Substances	DNA, Complementary ; IGF2BP2 protein, human ; IGF2BP2 protein, mouse ; Protein Isoforms ; RNA-Binding Proteins
Language	English
Publishing date	2012-03-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0033140
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Article ; Online: Acute knockdown of the insulin receptor or its substrates Irs1 and 2 in 3T3-L1 adipocytes suppresses adiponectin production.

Groeneveld, Matthijs P / Brierley, Gemma V / Rocha, Nuno M / Siddle, Kenneth / Semple, Robert K

Scientific reports

2016 Volume 6, Page(s) 21105

Abstract: Loss of function of the insulin receptor (INSR) in humans produces severe insulin resistance. Unlike "common" insulin resistance, this is associated with elevated plasma levels of the insulin-sensitising, adipose-derived protein adiponectin. The ... ...

Abstract	Loss of function of the insulin receptor (INSR) in humans produces severe insulin resistance. Unlike "common" insulin resistance, this is associated with elevated plasma levels of the insulin-sensitising, adipose-derived protein adiponectin. The underlying mechanism for this paradox is unclear, and it is at odds with the acute stimulation of adiponectin secretion reported on insulin treatment of cultured adipocytes. Given recent evidence for ligand-independent actions of the INSR, we used a lentiviral system to knock down Insr or its substrates Irs1 and Irs2 conditionally in 3T3-L1 murine preadipocytes/adipocytes to assess whether acute loss of their expression has different consequences to withdrawal of insulin. Efficient knockdown of either Insr or Irs1/2 was achieved by conditional shRNA expression, severely attenuating insulin-stimulated AKT phosphorylation and glucose uptake. Dual knockdown of Irs1 and Irs2 but not Insr in preadipocytes impaired differentiation to adipocytes. Acute knockdown of Insr or both Irs1 and Irs2 in adipocytes increased Adipoq mRNA expression but reduced adiponectin secretion, assessed by immunoassay. Knockdown sustained for 14 days also reduced immunoassay-detected adiponectin secretion, and moreover induced delipidation of the cells. These findings argue against a distinct effect of Insr deficiency to promote adiponectin secretion as the explanation for paradoxical insulin receptoropathy-related hyperadiponectinaemia.
MeSH term(s)	3T3-L1 Cells ; Adipocytes/metabolism ; Adiponectin/biosynthesis ; Adiponectin/genetics ; Animals ; Gene Expression Regulation ; Gene Knockdown Techniques ; Insulin Receptor Substrate Proteins/genetics ; Insulin Receptor Substrate Proteins/metabolism ; Mice ; Receptor, Insulin/genetics ; Receptor, Insulin/metabolism
Chemical Substances	Adiponectin ; Adipoq protein, mouse ; Insulin Receptor Substrate Proteins ; Irs1 protein, mouse ; Irs2 protein, mouse ; Receptor, Insulin (EC 2.7.10.1)
Language	English
Publishing date	2016-02-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep21105
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