Render Target: SSR
Render Timestamp: 2024-11-14T22:34:10.090Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-20 06:23:22.404
Product last modified at: 2024-10-29T23:45:08.027Z
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PDP - Template Name: Cell Extracts
PDP - Template ID: *******b5396df

NRF2 Control Cell Extracts #41645

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    Product Information

    Product Usage Information

    Boil for 3 minutes prior to use. Load 10 µL of untreated and MG-132 treated NRF2 Control Cell Extracts per lane.

    Storage

    Supplied in SDS Sample Buffer: 62.5 mM Tris-HCl (pH 6.8 at 25°C), 2% w/v SDS, 10% glycerol, 50 mM DTT, 0.01% w/v bromophenol blue or phenol red. Store at –20°C, or at –80°C for long-term storage.

    Product Description

    NRF2 Control Cell Extracts (A-172 untreated): Total cell extracts from A-172 cells serve as a negative control. Supplied in SDS Sample Buffer.

    NRF2 Control Cell Extracts (A-172 + MG-132): Total cell extracts from A-172 cells treated with MG-132 (10 μM, overnight) serve as a positive control.

    This lysate pair is produced as a control for western blotting of NRF2 protein.

    Background

    The nuclear factor-like 2 (NRF2) transcriptional activator binds antioxidant response elements (ARE) of target gene promoter regions to regulate expression of oxidative stress response genes. Under basal conditions, the NRF2 inhibitor INrf2 (also called KEAP1) binds and retains NRF2 in the cytoplasm where it can be targeted for ubiquitin-mediated degradation (1). Small amounts of constitutive nuclear NRF2 maintain cellular homeostasis through regulation of basal expression of antioxidant response genes. Following oxidative or electrophilic stress, KEAP1 releases NRF2, thereby allowing the activator to translocate to the nucleus and bind to ARE-containing genes (2). The coordinated action of NRF2 and other transcription factors mediates the response to oxidative stress (3). Altered expression of NRF2 is associated with chronic obstructive pulmonary disease (COPD) (4). NRF2 activity in lung cancer cell lines directly correlates with cell proliferation rates, and inhibition of NRF2 expression by siRNA enhances anti-cancer drug-induced apoptosis (5).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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