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Merck
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Fontos dokumentumok

M7449

Sigma-Aldrich

MG-132, Ready Made Solution

≥90% (HPLC)

Szinonimák:

MG-132 Proteasome Inhibitor

Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez


About This Item

EC-szám:
UNSPSC kód:
12352200
NACRES:
NA.32

Minőségi szint

Teszt

≥90% (HPLC)

form

DMSO solution

minőség

useful for proteasome inhibition

koncentráció

10 mM in DMSO

kiszállítva

dry ice

tárolási hőmérséklet

−20°C

Amino Acid Sequence

Z-Leu-Leu-Leu-al

Általános leírás

MG132 is a potent proteasome inhibitor that also inhibits calpains and lysosomal cathepsins. One of the first proteasome inhibitors to be developed, MG-132 is widely used in proteasome inhibition studies because of its high potency, high selectivity, and rapid reversibility. MG132 mechanistically acts as a proteasome inhibitor by hemiacetal formation with hydroxyl groups of active site threnonine residues.

Alkalmazás

MG-132, Ready Made Solution has been used to inhibit the proteasome in various systems, including:
  • hTERT-RPE1 and HeLa cells: Osorio-Zambrano, W.F. et al., PLoS One, 10(12), e0144434 (2015)
  • FaDu human hypopharynx cancer cells: Kim, S.-Y. et al., Autophagy, 14(3), 385-403 (2018)
  • HEK293 cells: Chen, Q. et al., Cell Reports, 22(11), 2860-2872 (2018).
  • Neonate rat cardiomyocytes: Turkieh, A. et al., Cell Death Dis., 10(8), 608 (2019)
  • Adult neural stem cells: Morrow, C.S. et al., Cell Stem Cell, 26(4), 558-568.e9 (2020).

Biokémiai/fiziológiai hatások

MG132, also known as carbobenzoxy-Leu-Leu-leucinal, is a peptide aldehyde which plays a vital role in the inhibition of proteolytic activity of the 26S proteasome complex. MG132 retards the growth of HeLa cells by promoting cell cycle arrest and apoptosis. Treatment of HepG2 and HeLa cells with MG-132 triggers increased expression of MCPIP1 mRNA, which in turn increases MCPIP1 protein concentration. MCPIP1 is implicated in negative regulation of macrophage activation and differentiation of several cell types, including pre-adipocytes, neuroprogenitor cells and osteoclast precursors. MG-132 stimulates dopamine reduction and nigral dopaminergic degeneration in both cell culture and animal models of Parkinson′s disease.
Potent, membrane-permeable proteasome inhibitor. Induces neurite outgrowth in PC12 cells at 10 μM. Blocks cleavage of poly(ADP-ribose) polymerase and apoptosis in thymocytes. Proteasome inhibition induces accumulation of heat shock protein mRNA, activation of heat-shock proteins, and enhanced thermotolerance in various cell types: however, it also activates JNK-1, which initiates apoptosis in response to cell stress.

Tulajdonságok és előnyök

  • Ready-to-use solution in DMSO
  • Purity tested by HPLC

Fizikai forma

MG-132, Ready Made Solution is supplied as a 10 mM (1 mg/210 μL) 0.2 μm-filtered solution in DMSO.

Tárolási osztály kódja

10 - Combustible liquids

WGK

WGK 2

Lobbanási pont (F)

188.6 °F - closed cup

Lobbanási pont (C)

87 °C - closed cup


Analitikai tanúsítványok (COA)

Analitikai tanúsítványok (COA) keresése a termék sarzs-/tételszámának megadásával. A sarzs- és tételszámok a termék címkéjén találhatók, a „Lot” vagy „Batch” szavak után.

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Dokumentumtár megtekintése

Proteasome inhibitor MG-132 induces dopaminergic degeneration in cell culture and animal models.
Sun F
Neurotoxicology, 27(5), 807-815 (2006)
RhoA Activation Sensitizes Cells to Proteotoxic Stimuli by Abrogating the HSF1-Dependent Heat Shock Response.
Meijering RA
PLoS ONE, 10(7), e0133553-e0133553 (2015)
Proteasome inhibitor MG-132 induces MCPIP1 expression.
Skalniak L
FEBS Journal, 280(11), 2665-2674 (2013)
Loss-of-function mutations in the ATP13A2/PARK9 gene cause complicated hereditary spastic paraplegia (SPG78).
Estrada-Cuzcano A
Brain, 140(Pt 2), 287-305 (2017)
Héctor Gálvez et al.
Frontiers in molecular neuroscience, 10, 321-321 (2017-11-07)
Atonal homolog 1 (Atoh1) and Neurogenin1 (Neurog1) are basic Helix-Loop-Helix (bHLH) transcription factors crucial for the generation of hair cells (HCs) and neurons in the inner ear. Both genes are induced early in development, but the expression of Atoh1 is

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