938077-77-1
Chemical Structure
ERα17p
Synonym(s): ERα (295-311)
- CAS 番号: 938077-77-1
- Formula:C84H154N24O23S
- Molecular Weight:1900.33
InChIKey: KBIGMLNABUOYNU-WBFOANKLSA-N
SMILES: O=C(N[C@@H](CC(C)C)C(N[C@@H](CCSC)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CCCCN)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CO)C(N[C@@H](CCCCN)C(N[C@@H](CCCCN)C(N[C@@H](CC(N)=O)C(N[C@@H](CO)C(N[C@@H](CC(C)C)C(N[C@@H](C)C(N[C@@H](CC(C)C)C(N[C@@H](CO)C(N[C@@H](CC(C)C)C(N[C@@H]([C@H](O)C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H]1NCCC1
Biological Activity: ERα17p (ERα 295-311) is the epitope of the CaM binding site on the estrogen receptor α (ER), which interacts with calmodulin (CaM) in a calcium-dependent manner. ERα17p regulates the migration of cancer cells MCF-7, SK-BR-3, T47D, and MDA-MB-231 through Rho/ROCK and PI3K/Akt signaling pathways. ERα17p inhibits proliferations of breast cancer cells, induces apoptosis, and inhibits tumor growth in mouse models[1][2][3].
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ERα17p | ERα17p (ERα 295-311) is the epitope of the CaM binding site on the estrogen receptor α (ER), which interacts with calmodulin (CaM) in a calcium-dependent manner. ERα17p regulates the migration of cancer cells MCF-7, SK-BR-3, T47D, and MDA-MB-231 through Rho/ROCK and PI3K/Akt signaling pathways. ERα17p inhibits proliferations of breast cancer cells, induces apoptosis, and inhibits tumor growth in mouse models. | |||||||||||||||||||||
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References
- [1]. Kampa M, et al., ERα17p, an ERα P295 -T311 fragment, modifies the migration of breast cancer cells, through actin cytoskeleton rearrangements. J Cell Biochem. 2011 Dec;112(12):3786-96. [Content Brief]
- [2]. Bourgoin-Voillard S, et al. Calmodulin association with the synthetic ERα17p peptide investigated by mass spectrometry[J]. International Journal of Mass Spectrometry, 2011, 305(2-3): 87-94.
- [3]. Pelekanou V, et al., The estrogen receptor alpha-derived peptide ERα17p (P(295)-T(311)) exerts pro-apoptotic actions in breast cancer cells in vitro and in vivo, independently from their ERα status. Mol Oncol. 2011 Feb;5(1):36-47. [Content Brief]
