Anti-TIN2 TINF2 Antibody

Product Name

Anti-TIN2 TINF2 Antibody

View all TIN2 Antibodies

SKU/Catalog Number

A03070

Size

100ul

Form

Liquid

Description

Boster Bio Anti-TIN2 TINF2 Antibody catalog # A03070. Tested in WB applications. This antibody reacts with Human,Mouse.

Storage & Handling

Store at -20°C for one year. For short term storage and frequent use, store at 4°C for up to one month. Avoid repeated freeze-thaw cycles.

Cite This Product

Anti-TIN2 TINF2 Antibody (Boster Biological Technology, Pleasanton CA, USA, Catalog # A03070)

Host

Rabbit

Contents

Rabbit IgG, 1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2

Clonality

Polyclonal

Isotype

IgG

Immunogen

Anti-Human RRM2B/p53R2 antibody was prepared by repeated immunizations with a synthetic peptide corresponding to a region near the N-terminus of human RRM2B1 protein. A residue of cysteine was added to facilitate coupling.

*Blocking peptide can be purchased. Costs vary based on immunogen length. Contact us for pricing.

Reactive Species

A03070 is reactive to TINF2 in Human, Mouse

Applications

A03070 is guaranteed for WB Boster Guarantee

Observed Molecular Weight

Calculated molecular weight

50023 MW

Background of TIN2

RRM2B/p53-R2, or p53-inducible ribonucleotide reductase small subunit 2-like protein, is a member of a broad superfamily of ferritin-like di-iron-carboxylate proteins. The RRM2B protein is an enzyme that catalyzes the conversion of ribonucleotides to deoxyribonucleotides that are essential for DNA synthesis, and is found in all eukaryotes. RRM2B plays a pivotal role in cell survival by repairing damaged DNA in a p53/TP53-dependent manner. It supplies deoxyribonucleotides for DNA repair in cells arrested at G1 or G2. It contains an iron-tyrosyl free radical center required for catalysis, and forms an active ribonucleotide reductase (RNR) complex with RRM1 which is expressed both in resting and proliferating cells in response to DNA damage. It is a heterotetramer with a large (RRM1) subunit, and interacts with p53/TP53. The interaction with RRM1 occurs in response to DNA damage and results in its translocation from cytoplasm to nucleus. It is widely expressed at a high level in skeletal muscle and at a weak level in thymus, and expressed in epithelial dysplasias and squamous cell carcinoma. Defects in RRM2B are the cause of encephalomyopathic mitochondrial depletion syndrome with renal tubulopathy (EMDSRT). Mitochondrial DNA depletion syndrome (MDS) is a clinically heterogeneous group of disorders characterized by a reduction in mitochondrial DNA (mtDNA) copy number. The encephalomyopathic form with renal tubulopathy is presented with various combinations of hypotonia, tubulopathy, seizures, respiratory distress, diarrhea, and lactic acidosis.

Antibody Validation

Boster validates all antibodies on WB, IHC, ICC, Immunofluorescence, and ELISA with known positive control and negative samples to ensure specificity and high affinity, including thorough antibody incubations.

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Assay Dilutions Recommendation

The recommendations below provide a starting point for assay optimization. The actual working concentration varies and should be decided by the user.

WB: 1:500-1:2000

Validation Images & Assay Conditions

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Figure 1. Western blotting validation for Anti-TIN2 TINF2 Antibody A03070

Western blot analysis of extracts of various cells

Gene/Protein Information For TINF2 (Source: Uniprot.org, NCBI)

Alternative Names

(TRF1)-interacting nuclear factor 2 variant 1; TERF1 (TRF1)-interacting nuclear factor 2; TERF1-interacting nuclear factor 2; TIN2TRF1-interacting nuclear protein 2 TINF2 DKCA3, TIN2 TERF1 interacting nuclear factor 2 TERF1-interacting nuclear factor 2|TERF1 (TRF1)-interacting nuclear factor 2|TRF1-interacting nuclear protein 2

For more info on TINF2, check out the TINF2 Infographic

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In this infographic, you will see the following information for TINF2: database IDs, superfamily, protein function, synonyms, molecular weight, chromosomal locations, tissues of expression, subcellular locations, post-translational modifications, and related diseases, research areas & pathways. If you want to see more information included, or would like to contribute to it and be acknowledged, please contact [email protected].

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