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SML1135

Sigma-Aldrich

MG-132(R)

≥95% (HPLC)

Synonyme(s) :

Z-L-Leu-D-Leu-L-Leu-al

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About This Item

Formule empirique (notation de Hill):
C26H41N3O5
Numéro CAS:
1211877-36-9
Poids moléculaire :
475.62
Numéro MDL:
MFCD28580122
Code UNSPSC :
12352200
ID de substance PubChem :
329825671
Nomenclature NACRES :
NA.32

Gamme de produits

SAFC Hitech®

Niveau de qualité

200

Pureté

≥95% (HPLC)

Forme

powder

Solubilité

DMSO: soluble

Température de stockage

−20°C

Chaîne SMILES 

O=C(N[C@H](CC(C)C)C(N[C@H](C=O)CC(C)C)=O)[C@H](CC(C)C)NC(OCC1=CC=CC=C1)=O

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

Clé InChI

TZYWCYJVHRLUCT-ZRBLBEILSA-N

Informations sur le gène

human ... CTSB(1508) , NFKB1(4790) , PSMA1(5682)

Catégories apparentées

Actions biochimiques/physiologiques

MG-132(R) is a potent, membrane-permeable proteasome inhibitor. It induces neurite outgrowth in PC12 cells at 10 M. MG-132(R) blocks cleavage of poly(ADP-ribose) polymerase and apoptosis in thymocytes. However, MG-132(R) also activates c-Jun N-terminal protein kinase (JNK-1), which initiates apoptosis in response to cell stress. Proteasome inhibition induces accumulation of heat shock protein mRNA, activation of heat-shock proteins, and enhanced thermotolerance in various cell types.

Informations légales

SAFC Hitech is a registered trademark of Sigma-Aldrich Co. LLC

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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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The effect of MG132, a proteasome inhibitor on HeLa cells in relation to cell growth, reactive oxygen species and GSH.
Han YH
Oncology Reports, 22(1), 215-221 (2009)
Yinfeng Xu et al.
FEBS letters, 593(15), 1974-1982 (2019-06-04)
The tumor protein p53-inducible nuclear protein 2 (TP53INP2) has been reported to participate in autophagy by interacting with autophagosome-localized autophagy-related protein 8 (Atg8) family proteins, including LC3. Here, we uncover a novel function for TP53INP2 in the autophagic degradation of
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Here we explore the relationship between presynaptic homeostatic plasticity and proteasome function at the Drosophila neuromuscular junction. First, we demonstrate that the induction of homeostatic plasticity is blocked after presynaptic proteasome perturbation. Proteasome inhibition potentiates release under baseline conditions but
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