RRM2 Antibody [L9E5] | Primary Antibodies

Application: Reactivity: Human

Lane 1: HDLM-2, Lane 2: PANC-1, Lane 3: THP-1

Usage Information

Dilution
WB1:1000 IHC1:100-1:400 IF1:400-1:1600

Application
WB, IHC, IF

Reactivity
Human

Source
Rabbit Monoclonal Antibody

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

Biological Description

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.

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
https://pubmed.ncbi.nlm.nih.gov/22632967/ https://pubmed.ncbi.nlm.nih.gov/31324785/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%