GnRH Associated Peptide (25-53), human
GnRH Associated Peptide (GAP) (25-53), human is the human gonadotropin-releasing hormone-associated peptide (GAP) 25-53 fragment (hGAP-25-53), can be used as immunogen to generate antiseras including MC-1, MC-2, and MC-3. GAP is joined to the luteinizing hormone-releasing hormone (LH-RH) sequence by a 3 amino acid processing site.
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- CAS. Nr.: 106061-19-2
- Formel: C140H226N40O49S
- Molecular Weight:3285.60
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
In Vitro
GAP (10 nM; 4 h) stimulates the release of both gonadotropins in anterior pituitaries from female Sprague-Dawley rats, but inhibits the basal secretion of prolactin by ~50%, compared with inhibition levels reported for dopamin, a known prolactin-inhibiting factor[2].
GAP (0.1-10 nM; 3-4 h) inhibits prolactin secretion by 40-45%, with an IC50 value of 0.25 nM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS. Nr. 106061-19-2
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Molecular Weight 3285.60
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Formel C140H226N40O49S
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Synonyms
GAP (25-53), human
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Sequence Shortening
FECTTHQPRSPLRDLKGALESLIEEETGQ
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
Reinheit & Dokumentation
Verweise
[1]. Culler MD, et al. Development of specific antisera and a radioimmunoassay procedure for the gonadotropin-releasing hormone associated peptide (GAP) of the LHRH prohormone. Brain Res Bull. 1986 Aug;17(2):219-23. [Content Brief]
[2]. Nikolics K, et al. A prolactin-inhibiting factor within the precursor for human gonadotropin-releasing hormone. Nature. 1985 Aug 8-14;316(6028):511-7. [Content Brief]
Calculators
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