Developmental regulation of insulin receptor gene in sciatic nerves and role of insulin on glycoprotein P0 in the Schwann cells

A single insulin receptor (InR) gene has been identified and extensively studied in model species ranging from nematodes to mice. However, most insects possess additional copies of InR, yet the functional significance, if any, of alternate InRs is unknown. Here, we used the wing-dimorphic brown planthopper (BPH) as a model system to query the role of a second InR copy in insects. NlInR2 resembled the BPH InR homologue (NlInR1) in terms of nymph development and reproduction, but revealed distinct regulatory roles in fuel metabolism, lifespan, and starvation tolerance. Unlike a lethal phenotype derived from NlInR1 null, homozygous NlInR2 null mutants were viable and accelerated DNA replication and cell proliferation in wing cells, thus redirecting short-winged–destined BPHs to develop into long-winged morphs. Additionally, the proper expression of NlInR2 was needed to maintain symmetric vein patterning in wings. Our findings provide the first direct evidence for the regulatory complexity of the two InR paralogues in insects, implying the functionally independent evolution of multiple InRs in invertebrates.

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Insulin receptor gene expression during development: developmental regulation of insulin receptor mRNA abundance in embryonic rat liver and yolk sac, developmental regulation of insulin receptor gene splicing, and comparison to abundance of insulin-like growth factor 1 receptor mRNA

Molecular Endocrinology ◽

10.1210/me.6.10.1665 ◽

1992 ◽

Vol 6 (10) ◽

pp. 1665-1672 ◽

Cited By ~ 8

Author(s):

S. J. Giddings

Keyword(s):

Gene Expression ◽

Growth Factor ◽

Insulin Receptor ◽

Developmental Regulation ◽

Receptor Gene ◽

Insulin Receptor Gene ◽

Gene Splicing ◽

Receptor Mrna ◽

Insulin Receptor Gene Expression ◽

Receptor Gene Expression

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Role of the exon 11 of the insulin receptor gene on insulin binding identified by anti-peptide antibodies

Molecular and Cellular Endocrinology ◽

10.1016/0303-7207(94)90226-7 ◽

1994 ◽

Vol 101 (1-2) ◽

pp. 121-127 ◽

Cited By ~ 9

Author(s):

Giorgio Sesti ◽

Antonella Nadia Tullio ◽

Maria Adelaide Marini ◽

Ernesto Manera ◽

Patrizia Borboni ◽

...

Keyword(s):

Insulin Receptor ◽

Receptor Gene ◽

Insulin Binding ◽

Insulin Receptor Gene ◽

Exon 11 ◽

Peptide Antibodies

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UNDERSTANDING THE ROLE OF VAYU AND AKASH MAHABHUTA IN THE MUTATIONS IN TYROSINE KINASE PORTION OF INSULIN RECEPTOR GENE FOUND IN NIDDM PATIENTS.

National Journal of Research in Ayurved Science ◽

10.52482/ayurlog.v6i3.90 ◽

2018 ◽

Vol 6 (3) ◽

Author(s):

Sneha Pramod Shinde

Keyword(s):

Amino Acids ◽

Tyrosine Kinase ◽

Insulin Receptor ◽

Receptor Gene ◽

Missense Mutations ◽

Insulin Receptor Gene ◽

Established Fact ◽

Niddm Patients

Abstract Normally, when insulin binds to the extracellular alpha chain of the insulin-receptor, it originates a change within receptorâ€™s structure, resulting in autophosphorylation of particular tyrosines in the cytoplasmic part of the beta chains. This change causes an initiation of a multifaceted cascade, which lastly results in secretion of the insulin. It is a well-known fact that the determination of any function of a protein is dependent on the sequence of the amino acids. Obviously any changes in the sequence result in differed function. This change is called as mutation. It is an established fact that missense mutations in the tyrosine kinase portion of the insulin receptor gene are present in patients with NIDDM. This mutation in the insulin-receptor prevents the relay of the stimuli, resulting in inhibition of insulin secretion finally. Here, we have demonstrated that the mutations in tyrosine kinase portion of insulin receptor gene found in the patients of NIDDM, are actually the derangement in the ruksa, laghu attributes, which are due to the combination of Vayu mahabhuta and Akash mahabhuta. We have also concluded that the replacement of Vayu mahabhuta and Akash mahabhuta by Prithvi mahabhuta and Jala mahabhuta, is the backbone of the pathology in NIDDM.

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