IGF-2 Lr3 Kit Receptor 1200mcg

IGF-2 Lr3 Kit Receptor 1200mcg

Brand: Full Catalog
Product Code: GK54
Availability:
In Stock
Price: $145.00
Description

This is a bulk discount for 10 vials of IGF-2 Lr3 (receptor grade) 10 vials (total 1200mg).

IGF-2 LR3, also called IGF-2 long arginine, and IGF-2 long R3, is a modified synthetic version of the endogenous growth factor insulin-like growth factor 2. Like insulin-like growth factor 1 (IGF-1) and relaxin, IGF-2 shares structural and other similarities to insulin[1][2]. IGF-2 binds to both the IGF-1 and IGF-2 receptor, displaying an agonistic relationship in the former case and in the latter acting as a signaling antagonist for IGF-1 receptor activity[1][2][3][4]. The “long arginine” modification allows IGF-2 LR3, like IGF-1 LR3, to survive longer in plasma.

The IGF-2 gene is heritable only from the father and is epigenetically imprinted, being heavily influenced by methylation and histone modification[1][2].Supraphysiological levels of IGF-2 appear to cause hypoglycemia, which is also the mechanism behind Doege-Potter syndrome (when IGF-2 is overproduced by tumor cells).

Chu et al (2005) find IGF-2 may be useful in preventing myocardial apoptosis following heart failure:


Our results revealed that IGF-II synergistically increased the cell apoptosis induced by suppressing of IGF-IR in neonatal rat ventricular myocytes. After binding of Leu27IGF-II, IGF-IIR became associated with alpha-q polypeptide, acted like a protein-coupled receptor to activate calcineurin, led to the translocation of Bad into mitochondria and release of cytochrome c into cytoplasm, and contributed to mitochondrial-dependent apoptosis in neonatal rat ventricular myocytes. Furthermore, inhibition of IGF-IIR, alpha-q polypeptide, or calcineurin by RNA interference could block the Leu27IGF-II-induced cell apoptosis. Together, this study provides a new insight into the effects of the IGF-IIR and its downstream signaling in myocardial apoptosis. Suppression of IGF-IIR signaling pathways may be a good strategy for both the protection against myocardial cell apoptosis and the prevention of heart failure progression.[5]

Thus far IGF-2 appears to be most active and important during development[6], but Tong et al (2009) speculate that, since IGF-1 and IGF-2 resistance may be a mechanism of dementia, IGF-1 and IGF-2 may be useful in treating or slowing dementia or related neurodegenerative disorders[7].

Citations
[1]Firth, S M; Ganeshprasad U, Baxter R C (Jan. 1998). "Structural determinants of ligand and cell surface binding of insulin-like growth factor-binding protein-3". J. Biol. Chem. USA 273 (5): 2631–8.
[2]Cubbage ML, Suwanichkul A, Powell DR (July 1990). "Insulin-like growth factor binding protein-3. Organization of the human chromosomal gene and demonstration of promoter activity". J. Biol. Chem. USA 265 (21): 12642–9.
[3]Storch, S; Kübler B, Höning S, Ackmann M, Zapf J, Blum W, Braulke T (Dec. 2001). "Transferrin binds insulin-like growth factors and affects binding properties of insulin-like growth factor binding protein-3". FEBS Lett. (NL) 509 (3): 395–8.
[4]Buckway, C K; Wilson E M, Ahlsén M, Bang P, Oh Y, Rosenfeld R G (Oct. 2001). "Mutation of three critical amino acids of the N-terminal domain of IGF-binding protein-3 essential for high affinity IGF binding". J. Clin. Endocrinol. Metab. USA 86 (10): 4943–50.
[5]Chu CH, Tzang BS, Chen LM, Liu CJ, Tsai FJ, Tsai CH, Lin JA, Kuo WW, Bau DT, Yao CH, Huang CY. Activation of insulin-like growth factor II receptor induces mitochondrial-dependent apoptosis through G(alpha)q and downstream calcineurin signaling in myocardial cells.Endocrinology. 2009 Jun;150(6):2723-31.
[6]Napoli I, Blusztajn JK, Mellott TJ.  Prenatal choline supplementation in rats increases the expression of IGF2 and its receptor IGF2R and enhances IGF2-induced acetylcholine release in hippocampus and frontal cortex. Brain Res. 2008 Oct 27;1237:124-35.
[7]Tong M, Dong M, de la Monte SM. Brain insulin-like growth factor and neurotrophin resistance in Parkinson's disease and dementia with Lewy bodies: potential role of manganese neurotoxicity.  J Alzheimers Dis. 2009 Mar;16(3):585-99.

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