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Fibroblast Growth Factor 19 (FGF19)

Cat no: F4212-91D

Fibroblast Growth Factor 19 (FGF19)

The FGFs are a family of more than 20 small (~17-26kD) secreted peptides. The initial characterization of these proteins focused on their ability to stimulate fibroblast proliferation. This mitogenic activity was mediated through FGF receptors (FGFRs) 1, 2, or 3. A fourth closely related tyrosine kinase receptor (FGFR4) was able to bind the FGFs but did not lead to a mitogenic response. FGFs modulate cellular activity via at least 5 distinct subfamilies of high-affinity FGF receptors (FGFRs): FGFR-1, -2, -3, and -4, all with intrinsic tyrosine kinase \nactivity and, except for FGFR-4, multiple splice isoforms, and FGFR-5, which lacks an intracellular kinase domain. There is growing evidence that FGFRs can be important for regulation of glucose and lipid homeostasis. The overexpression of a dominant negative form of FGFR-1 in beta cells leads to diabetes in mice, which thus implies that proper FGF signaling is required for normal beta cell function and glycemia maintenance. FGFR-2 appears to be a key molecule during pancreatic development. Moreover, FGFR-4 has been implicated in cholesterol metabolism and bile acid synthesis. FGF-19, has been shown to cause resistance to diet-induced obesity and insulin desensitization and to improve insulin, glucose, and lipid profiles in diabetic rodents. Since these effects, at least in part, are mediated through the observed changes in metabolic rates, FGF-19 can be considered as a regulator of energy expenditure. FGF-21 is preferentially expressed in liver, but an exact knowledge of FGF-21 bioactivity and its mode of action have been lacking to date. FGF-21 is a potent activator of glucose uptake on adipocytes, protects animals from diet-induced obesity when overexpressed in transgenic mice, and lowers blood glucose and triglyceride levels when therapeutically administered to diabetic rodents. \n\nApplications:\nSuitable for use in ELISA and Western Blot. Other applications not tested.\n\nRecommended Dilution:\nOptimal dilutions to be determined by the researcher.\n\nStorage and Stabillty:\nLyophilized powder may be stored at -20 degrees C. Stable for 12 months at -20 degrees C. Reconstitute with sterile ddH2O or PBS. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. Reconstituted product is stable for 12 months at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

F4212-91D

Size

100ug

Applications

ELISA, WB

Hosts

Rabbit

Reactivities

Hum

Form

Supplied as a lyophilized powder in PBS, pH 7.2. No preservative added. Reconstitute with 100ul sterile dH2O. Let the lyophilized pellet dissolve completely.

P Type

Pab

Purity

Purified by Immunoaffinity chromatography.

Isotype

IgG

References

1. Nicholes K, Guillet S, Tomlinson E, Hillan K, Wright B, Frantz GD, Pham TA, Dillard-Telm L, Tsai SP, \nStephan JP, Stinson J, Stewart T, French DM. A mouse model of hepatocellular carcinoma: ectopic \nexpression of fibroblast growth factor 19 in skeletal muscle of transgenic mice. Am J Pathol. \n2002 Jun;160(6):2295-307. \n2. Holt JA, Luo G, Billin AN, Bisi J, McNeill YY, Kozarsky KF, Donahee M, Wang da Y, Mansfield TA, \nKliewer SA, Goodwin B, Jones SA. Definition of a novel growth factor-dependent signal cascade \nfor the suppression of bile acid biosynthesis. Genes Dev. 2003 Jul 1;17(13):1581-91. Epub 2003 \nJun 18. \n3. Xie MH, Holcomb I, Deuel B, Dowd P, Huang A, Vagts A, Foster J, Liang J, Brush J, Gu Q, Hillan K, \nGoddard A, Gurney AL. FGF-19, a novel fibroblast growth factor with unique specificity for FGFR4. \nCytokine. 1999 Oct;11(10):729-35. \n4. Kharitonenkov A, Shiyanova TL, Koester A, Ford AM, Micanovic R, Galbreath EJ, Sandusky GE, \nHammond LJ, Moyers JS, Owens RA, Gromada J, Brozinick JT, Hawkins ED, Wroblewski VJ, Li DS, \nMehrbod F, Jaskunas SR, Shanafelt AB. FGF-21 as a novel metabolic regulator. J Clin Invest. 2005 \nJun;115(6):1627-35. Epub 2005 May 2. \n5. Fu L, John LM, Adams SH, Yu XX, Tomlinson E, Renz M, Williams PM, Soriano R, Corpuz R, Moffat \nB, Vandlen R, Simmons L, Foster J, Stephan JP, Tsai SP, Stewart TA. Fibroblast growth factor 19 \nincreases metabolic rate and reverses dietary and leptin-deficient diabetes. Endocrinology. 2004 \nJun;145(6):2594-603. Epub 2004 Feb 19. \nPage 2 of 3 (VERSION: 2009-10-21)\n6. Nishimura T, Nakatake Y, Konishi M, Itoh N. Identification of a novel FGF, FGF-21, preferentially \nexpressed in the liver. Biochim Biophys Acta. 2000 Jun 21;1492(1):203-6. \n7. Strack AM, Myers RW. Modulation of metabolic syndrome by fibroblast growth factor 19 \n(FGF19). Endocrinology. 2004 Jun;145(6):2591-3. Review. \n8. Nishimura T, Utsunomiya Y, Hoshikawa M, Ohuchi H, Itoh N. Structure and expression of a novel \nhuman FGF, FGF-19, expressed in the fetal brain. Biochim Biophys Acta. 1999 Jan 18;1444(1):148- \n51. \n9. Harmer NJ, Pellegrini L, Chirgadze D, Fernandez-Recio J, Blundell TL. The crystal structure of \nfibroblast growth factor (FGF) 19 reveals novel features of the FGF family and offers a structural \nbasis for its unusual receptor affinity. Biochemistry. 2004 Jan 27;43(3):629-40. \n10. Tomlinson E, Fu L, John L, Hultgren B, Huang X, Renz M, Stephan JP, Tsai SP, Powell-Braxton L, \nFrench D, Stewart TA. Transgenic mice expressing human fibroblast growth factor-19 display \nincreased metabolic rate and decreased adiposity. Endocrinology. 2002 May;143(5):1741-7.

Additional Info

Recognizes human FGF-19. \n

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