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Merck

474787

MG-132

≥95% (HPLC), proteasome inhibitor, powder

Synonyme(s) :

MG-132

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A propos de cet article

Formule empirique (notation de Hill) :
C26H41N3O5
Numéro CAS:
133407-82-6
Poids moléculaire :
475.62
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
MFCD00674886

Principaux documents

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Nom du produit

Z-Leu-Leu-Leu-al, Potent, reversible, and cell-permeable proteasome inhibitor (Ki = 4 nM).

SMILES string

[H]C(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC(C)C)NC(=O)OCc1ccccc1

InChI

1S/C26H41N3O5/c1-17(2)12-21(15-30)27-24(31)22(13-18(3)4)28-25(32)23(14-19(5)6)29-26(33)34-16-20-10-8-7-9-11-20/h7-11,15,17-19,21-23H,12-14,16H2,1-6H3,(H,27,31)(H,28,32)(H,29,33)/t21-,22-,23-/m0/s1

InChI key

TZYWCYJVHRLUCT-VABKMULXSA-N

assay

≥95% (HPLC)

form

powder

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

white

solubility

DMSO: 25 mg/mL
ethanol: 25 mg/mL

shipped in

ambient

storage temp.

−20°C

Quality Level

100

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Catégories apparentées

Disclaimer

Toxicity: Standard Handling (A)

General description

Potent, reversible, and cell-permeable proteasome inhibitor (Ki = 4 nM). Reduces the degradation of ubiquitin-conjugated proteins in mammalian cells and permeable stains of yeast by the 26S complex without affecting its ATPase or isopeptidase activities. Activates c-Jun N-terminal kinase (JNK1) which initiates apoptosis. Inhibits NF-κB activation (IC50 = 3 µM). This material is ≥95% pure by HPLC. A material with ≥98% purity by HPLC (Cat. No. 474790) is also available. Also available as a 20 mM solution in DMSO (Cat. No. 474788).

Other Notes

Steinhilb, M.L., et al. 2001. J. Biol. Chem.276, 4476.
Meriin, A.B., et al. 1998. J. Biol. Chem. 273, 6373.
Adams, J., and Stein, R. 1996. Ann. Rep. Med. Chem.31, 279.
Klafki, H.W., et al. 1996. J. Biol. Chem.271, 2865.
Lee, D.H., and Goldberg, A.L., 1996. J. Biol. Chem.271, 27280.
Wiertz, E.J., et al. 1996. Cell84, 769.
Jensen, T.J., et al. 1995. Cell 83, 129.
Read, M.A., et al. 1995. Immunity2, 493.
Rock, K.L., et al. 1994. Cell 78, 761.

Packaging

Packaged under inert gas

Preparation Note

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Classe de stockage

11 - Combustible Solids

wgk

WGK 3

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Haiyun Chen et al.
Clinical and translational medicine, 12(4), e574-e574 (2022-04-08)
Senescence-associated pathological cardiac hypertrophy (SA-PCH) is associated with upregulation of foetal genes, fibrosis, senescence-associated secretory phenotype (SASP), cardiac dysfunction and increased morbidity and mortality. Therefore, we conducted experiments to investigate whether GATA4 accumulation induces SA-PCH, and whether Bmi-1-RING1B promotes GATA4
Harihar Milaganur Mohan et al.
The Journal of biological chemistry, 295(49), 16754-16772 (2020-09-27)
α1-antitrypsin (AAT) regulates the activity of multiple proteases in the lungs and liver. A mutant of AAT (E342K) called ATZ forms polymers that are present at only low levels in the serum and induce intracellular protein inclusions, causing lung emphysema
Shuiyan Wu et al.
Cancer cell international, 21(1), 230-230 (2021-04-24)
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive disease with a high risk of induction failure and poor outcomes, with relapse due to drug resistance. Recent studies show that bromodomains and extra-terminal (BET) protein inhibitors are promising anti-cancer agents. ARV-825
Tanmoy Mondal et al.
EMBO molecular medicine, 13(3), e12716-e12716 (2021-02-16)
Lack of effective immune infiltration represents a significant barrier to immunotherapy in solid tumors. Thus, solid tumor-enriched death receptor-5 (DR5) activating antibodies, which generates tumor debulking by extrinsic apoptotic cytotoxicity, remains a crucial alternate therapeutic strategy. Over past few decades
Shihu Gan et al.
RNA biology, 18(6), 900-913 (2020-10-16)
The mechanisms that regulate cell-cycle arrest of cardiomyocytes during heart development are largely unknown. We have previously identified Tudor staphylococcal nuclease (Tudor-SN) as a cell-cycle regulator and have shown that its expression level was closely related to cell-proliferation capacity. Herein
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