在ner中，dna损伤结合蛋白2（ddb2，p48）与ddb1形成复合物，可以识别uv诱导的环丁烷嘧啶二聚体（cpd）。xpc和hrad23b形成的二聚体可识别紫外线诱导的6-4pp（另一种嘧啶二聚体）。rpa-xpa复合体识别6-4pp和顺铂损伤等。

Here, we report the identification of a p53 response element in the human DDB2 gene and demonstrate binding and direct transcriptional activation of the DDB2 gene by p53. We also show that the mouse DDB2 gene does not contain a functional p53 response element, providing an explanation for the deficiencies of UV-DDB and GGR in mice.

2009年6月30日 · In cells exposed to low doses of UV irradiation, DDB2 enhances nuclear accumulation of DDB1, which binds to a modified form of p53 phosphorylated at Ser-18 (p53 S18P) and, together with Cul4A, targets it for degradation.

ddb2通过诱导nf-κb的抑制剂iκba的转录，提高iκba的水平从而减少nf-κb的表达，并且ddb2的过表达会减少靶蛋白基质金属蛋白酶（mmp）的表达。 在结肠癌中，DDB2也通过抑制EMT从而减弱肿瘤的侵袭能力 [ 17 ] 。

2022年10月3日 · Recent mechanistic studies have shown that DDB2 prevents UV-induced skin cancer by increasing p53-mediated apoptosis of UV-damaged cells and maintaining high levels of ROS to induce premature senescence.

2020年7月25日 · This study demonstrates that the major alkaloid of the areca nut, arecoline, downregulated DDB2 expression through inhibiting p53’s DNA-binding (DB) activity toward the DDB2 promoter; however, p53’s transactivation (TA) domain was not affected by arecoline.

2020年7月25日 · Here we demonstrated that arecoline suppressed the expression of DDB2, which is transcriptionally regulated by p53 and is required for nucleotide excision repair (NER). Ectopic expression of DDB2 restored NER activity in arecoline-treated cells, suggesting that DDB2 downregulation was critical for arecoline-mediated NER inhibition.

the data indicate that p53-dependent upregulation of XPC and DDB2 is a key mechanism upon genotoxic stress, whereby melanoma cells acquire resistance towards DNA cross-linking agents. DDB2 and a DDB2-ATM feedback loop influence HCMV replication.

We propose that both before and after UV irradiation, DDB2 directly regulates p53 levels, while DDB2 expression is itself regulated by p53. Tumor suppressor p53 controls cell cycle progression and apoptosis following DNA damage, thus minimizing carcinogenesis. Mutations in the human DDB2 gene generate the E subgroup of xeroderma pigmentosum (XP-E).

The DDB2 gene, which is mutated in xeroderma pigmentosum group E, enhances global genomic repair of cyclobutane pyrimidine dimers and suppresses UV-induced mutagenesis. Because DDB2 transcription increases after DNA damage in a p53-dependent manner, we searched for and found a region in the human DD …