KISS1 Antibody (N-Term)
Purified Rabbit Polyclonal Antibody (Pab)
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Application ![]()
| WB, IHC-P, E |
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Primary Accession | Q15726 |
Reactivity | Human |
Host | Rabbit |
Clonality | polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 14705 Da |
Gene ID | 3814 |
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Other Names | Metastasis-suppressor KiSS-1, Kisspeptin-1, Metastin, Kisspeptin-54, Kisspeptin-14, Kisspeptin-13, Kisspeptin-10, KISS1 |
Target/Specificity | This KISS1 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 20-52 amino acids from human KISS1. |
Dilution | WB~~1:2000 IHC-P~~1:100~500 E~~Use at an assay dependent concentration. |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | KISS1 Antibody (N-Term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | KISS1 |
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Function | Metastasis suppressor protein in malignant melanomas and in some breast cancers. May regulate events downstream of cell-matrix adhesion, perhaps involving cytoskeletal reorganization. Generates a C- terminally amidated peptide, metastin which functions as the endogenous ligand of the G-protein coupled receptor GPR54. Activation of the receptor inhibits cell proliferation and cell migration, key characteristics of tumor metastasis. Kp-10 is a decapeptide derived from the primary translation product, isolated in conditioned medium of first trimester trophoblast. Kp-10, but not other kisspeptins, increased intracellular Ca(2+) levels in isolated first trimester trophoblasts. Kp-10 is a paracrine/endocrine regulator in fine-tuning trophoblast invasion generated by the trophoblast itself. The receptor is also essential for normal gonadotropin-released hormone physiology and for puberty. The hypothalamic KiSS1/GPR54 system is a pivotal factor in central regulation of the gonadotropic axis at puberty and in adulthood. |
Cellular Location | Secreted. |
Tissue Location | Very high expression in placenta, with the next highest level in testis and moderate levels in pancreas, liver, small intestine and brain at much lower levels. Expression levels increased in both early placentas and molar pregnancies and are reduced in choriocarcinoma cells. Expressed at higher levels in first trimester trophoblasts than at term of gestation, but only expressed in the villous trophoblast. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Metastasis suppressor protein in malignant melanomas and in some breast cancers. May regulate events downstream of cell- matrix adhesion, perhaps involving cytoskeletal reorganization. Generates a C-terminally amidated peptide, metastin which functions as the endogenous ligand of the G-protein coupled receptor GPR54. Activation of the receptor inhibits cell proliferation and cell migration, key characteristics of tumor metastasis. Kp-10 is a decapeptide derived from the primary translation product, isolated in conditioned medium of first trimester trophoblast. Kp-10, but not other kisspeptins, increased intracellular Ca(2+) levels in isolated first trimester trophoblasts. Kp-10 is a paracrine/endocrine regulator in fine- tuning trophoblast invasion generated by the trophoblast itself. The receptor is also essential for normal gonadotropin-released hormone physiology and for puberty. The hypothalamic KiSS1/GPR54 system is a pivotal factor in central regulation of the gonadotropic axis at puberty and in adulthood.
REFERENCES
Lee J.-H.,et al.J. Natl. Cancer Inst. 88:1731-1737(1996).
Lee J.-H.,et al.J. Natl. Cancer Inst. 89:1549-1549(1997).
West A.,et al.Genomics 54:145-148(1998).
Qiao C.,et al.Submitted (JUN-2002) to the EMBL/GenBank/DDBJ databases.
Wan D.,et al.Proc. Natl. Acad. Sci. U.S.A. 101:15724-15729(2004).

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