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Anti-Mre11 Rabbit Antibody [B17H15]

Catalog No.: F4059

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 IHC1:2000 FCM1:500

Application
WB, IHC, FCM, ChIP

Reactivity
Human, Mouse, Rat

Source
Rabbit

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 Observed MW
81 kDa 81 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human fetal kidney; Human colon; Human endometrial carcinoma; Human breast carcinoma; Mouse testis; Mouse brain; Rat brain; Rat colon; K562; Jurkat; HEK-293T; D3; C6; RAW 264.7; PC-12; NIH/3T3; HeLa
Negative Control

Datasheet & SDS

Biological Description

Specificity
Mre11 Rabbit mAb detects endogenous levels of Mre11 protein.

Clone
B17H15

Synonym(s)
HNGS1, MRE11A, MRE11, Double-strand break repair protein MRE11, Meiotic recombination 11 homolog 1, Meiotic recombination 11 homolog A, MRE11 homolog 1, MRE11 homolog A

Background
Mre11 is an evolutionarily conserved nuclease and core component of the Mre11-Rad50-Nbs1 (MRN) complex, which is essential for DNA double-strand break (DSB) repair, telomere maintenance, and DNA damage signaling. Structurally, Mre11 contains an N-terminal nuclease domain composed of five conserved phosphoesterase motifs that coordinate two metal ions to mediate endo- and exonuclease activities, as well as a C-terminal region with DNA-binding domains that facilitate substrate recognition. It is ubiquitously expressed across all kingdoms of life, reflecting its fundamental role in genome stability. Functionally, Mre11 performs Mn²⁺-dependent nucleolytic processing of DNA ends, including single-stranded endonuclease, double-stranded exonuclease, and hairpin-opening activities, and works with Rad50 and Nbs1 to couple DNA repair with cell cycle checkpoint activation. Mutations in human Mre11 cause ataxia telangiectasia-like disorder (ATLD), highlighting its importance in maintaining chromosomal integrity.

Background

Mre11 is an evolutionarily conserved nuclease and core component of the Mre11-Rad50-Nbs1 (MRN) complex, which is essential for DNA double-strand break (DSB) repair, telomere maintenance, and DNA damage signaling. Structurally, Mre11 contains an N-terminal nuclease domain composed of five conserved phosphoesterase motifs that coordinate two metal ions to mediate endo- and exonuclease activities, as well as a C-terminal region with DNA-binding domains that facilitate substrate recognition. It is ubiquitously expressed across all kingdoms of life, reflecting its fundamental role in genome stability. Functionally, Mre11 performs Mn²⁺-dependent nucleolytic processing of DNA ends, including single-stranded endonuclease, double-stranded exonuclease, and hairpin-opening activities, and works with Rad50 and Nbs1 to couple DNA repair with cell cycle checkpoint activation. Mutations in human Mre11 cause ataxia telangiectasia-like disorder (ATLD), highlighting its importance in maintaining chromosomal integrity.

References
https://pubmed.ncbi.nlm.nih.gov/15047855/

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

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
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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%