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SML1135

Sigma-Aldrich

MG-132(R)

≥95% (HPLC)

Synonym(e):

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

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About This Item

Empirische Formel (Hill-System):
C26H41N3O5
CAS-Nummer:
1211877-36-9
Molekulargewicht:
475.62
MDL-Nummer:
MFCD28580122
UNSPSC-Code:
12352200
PubChem Substanz-ID:
329825671
NACRES:
NA.32

Produktlinie

SAFC Hitech®

Qualitätsniveau

200

Assay

≥95% (HPLC)

Form

powder

Löslichkeit

DMSO: soluble

Lagertemp.

−20°C

SMILES String

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

InChIKey

TZYWCYJVHRLUCT-ZRBLBEILSA-N

Angaben zum Gen

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

Verwandte Kategorien

Biochem./physiol. Wirkung

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.

Rechtliche Hinweise

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

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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SN50 trifluoroacetate salt ≥95% (HPLC)

Sigma-Aldrich

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ALLN Cell-permeable inhibitor of calpain I (Ki = 190 nM), calpain II (Ki = 220 nM), cathepsin B (Ki = 150 nM), and cathepsin L (Ki = 500 pM).

Sigma-Aldrich

208719

ALLN

Xueyan Zhao et al.
Developmental and comparative immunology, 106, 103632-103632 (2020-01-29)
Tightly regulation of NF-κB signaling is essential to innate and adaptive immune responses, but its regulatory mechanism remains unclear in various organisms, especially teleost fish. In this study, we reported that IRF3 attenuates the inhibitory effect of IκBα on NF-κB
Shashipavan Chillappagari et al.
Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 20(1), 140-148 (2020-06-15)
The stress-regulated enzyme hemeoxygenase-1 (HO-1) contributes to the cell response towards inflammation and oxidative stress. We previously reported on curtailed HO-1 expression in cystic fibrosis (CF) bronchial epithelial (CFBE41o-) cells and CF-mice, but the molecular mechanisms for this are not
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Nature communications, 9(1), 267-267 (2018-01-20)
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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Serine tRNAs (tRNASer) are frequently overexpressed in tumors and associated with poor prognosis and increased risk of recurrence in breast cancer. Impairment of tRNA biogenesis and abundance also impacts proteome homeostasis, and activates protein quality control systems. Herein, we aimed
Fanjie Jin et al.
Oncology letters, 19(1), 858-868 (2020-01-04)
The clinical significance of the proteasome inhibitor MG132 has been examined in numerous human cancer types; however, its influence on the metastasis and progression of pancreatic cancer is yet to be determined. In the present study, the effect of MG132
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