Choose Your Country or Region

Anti-DDB-2 Rabbit Antibody [M14F11]

Catalog No.: F1449

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000

Application
WB

Reactivity
Human

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
43 kDa

Datasheet & SDS

Biological Description

Specificity
Anti-DDB-2 Rabbit Antibody [M14F11] detects endogenous levels of total DDB-2 protein.

Clone
M14F11

Synonym(s)
DNA damage-binding protein 2; DDB p48 subunit (DDBb); Damage-specific DNA-binding protein 2; UV-damaged DNA-binding protein 2 (UV-DDB 2); DDB2

Background
DDB2 (Damage-specific DNA-binding protein 2) is a protein encoded by the human DDB2 gene located on chromosome 11p12-p11. It plays a vital role in the nucleotide excision repair (NER) pathway, where it recognizes and binds to UV-induced DNA lesions to initiate repair. DDB2 contains several key domains: a terminal seven-bladed WD40 β-propeller domain responsible for DNA interaction, a disordered N-terminal tail rich in lysine residues that serve as ubiquitination sites, and a helix-loop-helix motif (residues 101–136) that interacts with DDB1 to form the UV-DDB complex, essential for damaged DNA recognition. Upon UV damage recognition, DDB2 activates the Cullin 4-RING ubiquitin ligase complex (CRL4^DDB2^), which ubiquitinates histones, XPC, and DDB2 itself, promoting chromatin remodeling and efficient repair. DDB2 levels fluctuate throughout the cell cycle: they rise during mid-G1, peak at the G1/S boundary, and decline during S phase, reflecting its role in DNA damage response and cell cycle regulation. The expression of DDB2 is tightly regulated: its transcription is activated by p53 and TAp63γ, while reactive oxygen species and AP1 transcription factors also induce its expression in a p53-independent manner. Post-translational modifications, including ubiquitination, phosphorylation by p38 MAPK, poly(ADP-ribosylation), and SUMOylation, dynamically regulate DDB2’s stability, chromatin binding, and repair functions. Additionally, DDB2 affects cell cycle progression by degrading inhibitors like p27 and CDT2 and stabilizing CDT1, which contributes to DNA replication licensing. Dysregulation of DDB2 has been linked to carcinogenesis, and its expression levels are associated with sensitivity to chemoradiotherapy.

Background

DDB2 (Damage-specific DNA-binding protein 2) is a protein encoded by the human DDB2 gene located on chromosome 11p12-p11. It plays a vital role in the nucleotide excision repair (NER) pathway, where it recognizes and binds to UV-induced DNA lesions to initiate repair. DDB2 contains several key domains: a terminal seven-bladed WD40 β-propeller domain responsible for DNA interaction, a disordered N-terminal tail rich in lysine residues that serve as ubiquitination sites, and a helix-loop-helix motif (residues 101–136) that interacts with DDB1 to form the UV-DDB complex, essential for damaged DNA recognition. Upon UV damage recognition, DDB2 activates the Cullin 4-RING ubiquitin ligase complex (CRL4^DDB2^), which ubiquitinates histones, XPC, and DDB2 itself, promoting chromatin remodeling and efficient repair. DDB2 levels fluctuate throughout the cell cycle: they rise during mid-G1, peak at the G1/S boundary, and decline during S phase, reflecting its role in DNA damage response and cell cycle regulation. The expression of DDB2 is tightly regulated: its transcription is activated by p53 and TAp63γ, while reactive oxygen species and AP1 transcription factors also induce its expression in a p53-independent manner. Post-translational modifications, including ubiquitination, phosphorylation by p38 MAPK, poly(ADP-ribosylation), and SUMOylation, dynamically regulate DDB2’s stability, chromatin binding, and repair functions. Additionally, DDB2 affects cell cycle progression by degrading inhibitors like p27 and CDT2 and stabilizing CDT1, which contributes to DNA replication licensing. Dysregulation of DDB2 has been linked to carcinogenesis, and its expression levels are associated with sensitivity to chemoradiotherapy.

References
https://pubmed.ncbi.nlm.nih.gov/25628365/ https://pubmed.ncbi.nlm.nih.gov/36190612/

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
If you have any other enquiries, please leave a message.

* Indicates a Required Field

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%