SML1135
MG-132(R)
≥95% (HPLC), membrane-permeable proteasome inhibitor, powder
동의어(들):
Z-L-Leu-D-Leu-L-Leu-al
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크기 선택
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제품정보 (DICE 배송 시 비용 별도)
실험식(Hill 표기법):
C26H41N3O5
CAS 번호:
Molecular Weight:
475.62
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.32
MDL number:
제품 이름
MG-132(R), ≥95% (HPLC)
product line
SAFC Hitech®
Quality Level
assay
≥95% (HPLC)
form
powder
solubility
DMSO: soluble
storage temp.
−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
InChI key
TZYWCYJVHRLUCT-ZRBLBEILSA-N
Gene Information
human ... CTSB(1508), NFKB1(4790), PSMA1(5682)
Biochem/physiol Actions
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.
Legal Information
SAFC Hitech is a registered trademark of Sigma-Aldrich Co. LLC
저장 등급
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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
Ling-Yun Chu et al.
Scientific reports, 7(1), 12472-12472 (2017-10-01)
Pro-inflammatory cytokines are known to induce endothelial cell autophagy, but the role of autophagy in regulating the expression of pro-inflammatory molecules has not been characterized. We hypothesized that autophagy facilitates expression of endothelial adhesion molecules. TNFα and IL-1β induced autophagy
Yalong Wang et al.
Neuroscience letters, 739, 135402-135402 (2020-09-26)
Synaptotagmin-11 (Syt11) is associated with schizophrenia and Parkinson's disease (PD) and is a critical substrate of parkin, an E3 ubiquitin ligase linked to PD. Previously we reported that Syt11 regulates multiple membrane trafficking pathways in neurons and glia. However, the
Corinna Wentzel et al.
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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