RRM2 Antibody [L9E5]

Catalog No.: F7845

    Application: Reactivity:
    • Lane 1: HDLM-2, Lane 2: PANC-1, Lane 3: THP-1
    1/

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    代表番号: 045-509-1970|電子メール:sales@selleck.co.jp

    使用情報

    Dilution
    1:1000
    1:100-1:400
    1:400-1:1600
    Application
    WB, IHC, IF
    Source
    Rabbit Monoclonal Antibody
    Reactivity
    Human
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    45 kDa

    Datasheet & SDS

    生物学的記述

    Specificity
    RRM2 Antibody [L9E5] detects endogenous levels of total RRM2 protein.
    Clone
    L9E5
    Synonym(s)
    Ribonucleoside-diphosphate reductase subunit M2; RRM2
    Background
    Ribonucleotide reductase small subunit M2 (RRM2) is a catalytic subunit of the ribonucleotide reductase heterodimer that governs the rate‑limiting step in the conversion of ribonucleotides to deoxyribonucleotides and thereby sets the size and composition of cellular dNTP pools required for DNA replication and repair. RRM2 contains a di‑iron centre and radical‑transfer pathway that drives the reduction of ribonucleotide diphosphates, and its activity is tightly coupled to the larger RRM1‑containing holoenzyme whose assembly and redox state tune RRM2‑dependent dNTP production across the cell cycle. RRM2 expression peaks in S phase and G2, and CDK‑mediated phosphorylation of RRM2 at Thr33 during G2 targets the subunit to the SCF–Cyclin F ubiquitin ligase for proteasomal degradation, thereby coupling cell‑cycle progression to RRM2 turnover and preventing dNTP pool imbalance and genome instability. RRM2 is overexpressed and supports sustained proliferation, migration, and chemoresistance by maintaining elevated dNTP levels and concurrently engaging pro‑survival and signaling pathways such as Bcl‑2–dependent apoptosis control and RRM2‑linked Wnt/β‑catenin or JAK2/STAT3 signaling, while depletion or pharmacological inhibition of RRM2 impairs tumor growth, enhances sensitivity to DNA‑damaging agents and targeted kinase inhibitors, and delays relapse in models of BRAF‑mutant melanoma and chemoresistant carcinomas.
    References

    技術サポート

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