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A6185

Calpain Inhibitor I

Name: Calpain Inhibitor I
Brand: SIGMA

synthetic (organic), ≥97% (TLC), cysteine protease inhibitor, powder

동의어(들):

ALLN, Ac-LLnL-CHO, MG-101, N-Acetyl-L-leucyl-L-leucyl-L-norleucinal, N-Acetyl-Leu-Leu-Norleu-al

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제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):

C₂₀H₃₇N₃O₄

CAS 번호:

110044-82-1

Molecular Weight:

383.53

NACRES:

NA.77

PubChem Substance ID:

24891066

UNSPSC Code:

12352200

MDL number:

MFCD00065505

Beilstein/REAXYS Number:

7656053

Assay:

≥97% (TLC)

Form:

powder

Quality level:

200

기술 서비스

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제품 이름

Calpain Inhibitor I, ≥97% (TLC), powder

biological source

synthetic (organic)

Quality Level

200

assay

≥97% (TLC)

form

powder

color

white

solubility

DMSO: soluble, ethanol: soluble

storage temp.

−20°C

SMILES string

[H]C(=O)[C@H](CCCC)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(C)=O

InChI

1S/C20H37N3O4/c1-7-8-9-16(12-24)22-19(26)18(11-14(4)5)23-20(27)17(10-13(2)3)21-15(6)25/h12-14,16-18H,7-11H2,1-6H3,(H,21,25)(H,22,26)(H,23,27)/t16-,17-,18-/m0/s1

InChI key

FMYKJLXRRQTBOR-BZSNNMDCSA-N

Gene Information

human ... CAPN1(823), CTSB(1508), PSMA1(5682)

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Application

Calpain Inhibitor I have been used:

as a component of protease inhibitor cocktail for gel shift analysis
for treating HeLa cell cultures
for inhibition of 26 S proteasome in 26 S proteasome inhibition assays

Biochem/physiol Actions

Can initiate apoptosis in HL-60 cells but blocks dexamethasone-induced apoptosis in thymocytes and cycloheximide-induced apoptosis in metamyelocytes. Inhibits cyclin B degradation and arrests the cell cycle at G₁/S and at meta-/anaphase. Blocks induction of nitric oxide synthase by LPS in macrophages.

Calpain Inhibitor I inhibits tumor necrosis factor-induced (TNF-induced) cleavage of Poly (ADP-ribose) polymerase (PARP) and calpastatin in apoptosis. It also inhibits oxygen/glucose deprivation (OGD) induced cleavage of caspase-12 and Bcl-xL..

저장 등급

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

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문서 라이브러리 방문

Cleavage of the calpain inhibitor, calpastatin, during apoptosis

Porn-Ares M I, et al.

Cell Death and Differentiation, 5(12), 1028-1028 (1998)

In vivo inhibition of cyclin B degradation and induction of cell-cycle arrest in mammalian cells by the neutral cysteine protease inhibitor N-acetylleucylleucylnorleucinal.

S W Sherwood et al.

Proceedings of the National Academy of Sciences of the United States of America, 90(8), 3353-3357 (1993-04-15)

The cytotoxic neutral cysteine protease inhibitor N-acetylleucylleucylnorleucinal (ALLN) inhibits cell-cycle progression in CHO cells, affecting the G1/S and metaphase-anaphase transition points, as well as S phase. Mitotic arrest induced by ALLN is associated with the inhibition of cyclin B degradation.

Inhibitors of the proteasome pathway interfere with induction of nitric oxide synthase in macrophages by blocking activation of transcription factor NF-kappa B.

J M Griscavage et al.

Proceedings of the National Academy of Sciences of the United States of America, 93(8), 3308-3312 (1996-04-16)

The objective of this study was to elucidate the role of the proteasome pathway or multicatalytic proteinase complex in the induction of immunologic nitric oxide (NO) synthase (iNOS) in rat alveolar macrophages activated by lipopolysaccharide. Macrophages were incubated in the

Calpain inhibitors and serine protease inhibitors can produce apoptosis in HL-60 cells.

Q Lu et al.

Archives of biochemistry and biophysics, 334(1), 175-181 (1996-10-01)

Recent investigations indicate that proteolysis is an important event in generation of the apoptosis phenotype. Although various proteases have been suggested to be candidates for this proteolysis, the results from different laboratories are inconsistent. In the present studies, HL-60 cells

Calpain activation in apoptosis.

M K Squìer et al.

Journal of cellular physiology, 159(2), 229-237 (1994-05-01)

Programmed cell death is an active process wherein the cell initiates a sequence of events culminating in the fragmentation of its DNA, nuclear collapse, and disintegration of the cell into small, membrane-bound apoptotic bodies. Examination of the death program in

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