N-Acetyl-Ser-Asp-Lys-Pro
CAS No. 127103-11-1
N-Acetyl-Ser-Asp-Lys-Pro ( —— )
Catalog No. M22966 CAS No. 127103-11-1
Acetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
Size | Price / USD | Stock | Quantity |
5MG | 91 | In Stock |
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10MG | 156 | In Stock |
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25MG | 321 | In Stock |
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50MG | 482 | In Stock |
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100MG | 696 | In Stock |
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200MG | Get Quote | In Stock |
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500MG | Get Quote | In Stock |
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1G | Get Quote | In Stock |
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Biological Information
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Product NameN-Acetyl-Ser-Asp-Lys-Pro
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NoteResearch use only, not for human use.
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Brief DescriptionAcetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?
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DescriptionAcetyl Ser-Asp-Lys-Pro is formed in bone marrow cells by enzymatic processing of thymosin β4. It inhibits the entry of pluripotent hemopoietic stem cells into S-phase of the cell cycle and protects against Ara-C lethality in mice.N-Acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a specific substrate for the N-terminal site of ACE and increases 5-fold during ACE inhibitor therapy.??AcSDKP inhibited the proliferation of isolated cardiac fibroblasts (P<0.05) but significantly stimulated the proliferation of vascular smooth muscle cells.?Flow cytometry of rat cardiac fibroblasts treated with AcSDKP showed significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle.?In cardiac fibroblasts transfected with a Smad-sensitive luciferase reporter construct, AcSDKP decreased luciferase activity by 55+/-9.7% (P=0.01).?Moreover, phosphorylation and nuclear translocation of Smad2 was decreased in cardiac fibroblasts treated with AcSDKP.?To conclude, AcSDKP inhibits the growth of cardiac fibroblasts and also inhibits TGFbeta1-stimulated phosphorylation of Smad2.?Because AcSDKP increases substantially during ACE inhibitor therapy, this suggests a novel pathway independent of angiotensin II, by which ACE inhibitors can inhibit cardiac fibrosis.
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Synonyms——
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PathwayEndocrinology/Hormones
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TargetRAAS
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RecptorACE
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Research Area——
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Indication——
Chemical Information
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CAS Number127103-11-1
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Formula Weight487.5
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Molecular FormulaC20H33N5O9
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Purity>98% (HPLC)
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Solubility——
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SMILESO=C([C@@H]1N(C([C@H](NC([C@@H](NC([C@H](NC(C)=O)CO)=O)CC(O)=O)=O)CCCCN)=O)CCC1)O
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1. Rousseau A, et al. The hemoregulatory peptide N-acetyl-Ser-Asp-Lys-Pro is a natural and specificsubstrate of the N-terminal active site of human angiotensin-converting enzyme. J Biol Chem. 1995 Feb 24;270(8):3656-61.
molnova catalog
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