ERCC2 antibody - N-terminal region (P100701_P050)
- Known as:
- ERCC2 (anti-) - N-terminal region (P100701_P050)
- Catalog number:
- p100701_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ERCC2 antibody - N-terminal region (P100701_P050)
Related genes to: ERCC2 antibody - N-terminal region (P100701_P050)
- Gene:
- ERCC2 NIH gene
- Name:
- ERCC excision repair 2, TFIIH core complex helicase subunit
- Previous symbol:
- XPD
- Synonyms:
- MAG, EM9, MGC102762, MGC126218, MGC126219, TFIIH
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: ERCC2 antibody - N-terminal region (P100701_P050)
Related articles to: ERCC2 antibody - N-terminal region (P100701_P050)
- Despite lacking melanin, vitiligo skin paradoxically exhibits a lower incidence of non-melanoma skin cancers, indicating alternative epidermal defense mechanisms. We investigated the protective role of microRNA-31-5p (miR-31-5p), which is elevated in vitiligo lesions, against UV-B-induced DNA damage in keratinocytes. Primary human keratinocytes exposed to UV-B were treated with miR-31-5p mimic or antagomiR. miR-31-5p mimic significantly reduced DNA damage and increased the expression of nucleotide excision repair genes (DDB1, ERCC2, XPC), while alleviating replication stress. SP1 was identified as a direct target of miR-31-5p, and its suppression mirrored the DNA-protective effects. Importantly, miR-31-5p mimic robustly activated autophagy, as shown by increased expression of autophagy markers and enhanced autophagic flux; bafilomycin treatment further elevated LC3B and Beclin levels, indicating augmented autophagosome accumulation. Inhibition of autophagy with a ULK1 inhibitor abrogated the DNA-protective effects mediated by miR-31-5p mimic, confirming autophagy's essential role. Analysis of lesional vitiligo epidermis revealed elevated miR-31-5p and reduced SP1 expression, consistent with in vitro findings. Our study identifies a novel miR-31-5p-SP1-autophagy-DNA repair axis in UV-B-exposed keratinocytes, providing new insight into melanin-independent epidermal protection in vitiligo and potential therapeutic strategies for enhancing UV resistance. - Source: PubMed
Publication date: 2026/06/02
Chowdhary ManishRaina ArunPriya AnshuKundu AktaGupta AayushSingh Archana - Trimodality therapy (TMT)-maximal transurethral resection of bladder tumor (TURBT) followed by concurrent chemoradiotherapy-can offer oncologic outcomes comparable to radical cystectomy (RC) in carefully selected muscle-invasive bladder cancer (MIBC) patients while preserving the bladder and, possibly, the quality of life. Systematic reviews and long-term series support durable bladder-intact survival in responders, yet there is still a significant percentage of patients who exhibit incomplete response or invasive intravesical recurrence requiring salvage RC. This review covers computational genomics, transcriptomics, immune contexture, radiogenomics, and digital pathology approaches for predicting response in order to avoid preventable TMT failures. We discuss clinically relevant endpoints (complete response, invasive recurrence, bladder-intact survival, and salvage RC), patient selection (carcinoma in situ, hydronephrosis, debulking feasibility, and histology), and DNA damage response (DDR) biology-highlighting and related pathways as determinants of chemo-radiation sensitivity. We then review reproducible transcriptomic subtype classifiers and immune deconvolution methods, emphasizing translational constraints and reporting standards. Finally, we propose an integrated hypothetical modeling framework (calibration, external validation, and decision-curve thresholds) to guide recommendations for upfront RC versus bladder preservation with intensified surveillance and timely salvage RC. - Source: PubMed
Publication date: 2026/05/16
Schițcu Vlad-HoriaMunteanu Vlad CristianBorz Mihnea BogdanCojocaru IonMorari OctaviaGîrbovan MirceaTișe Andrei-Ionuț - Xeroderma pigmentosum group B (XPB/ERCC3) and group D (XPD/ERCC2) helicases are integral components of the transcription factor IIH (TFIIH) complex, coordinating DNA unwinding during transcription initiation and nucleotide excision repair (NER). XPB functions as an ATP-driven translocase that generates torsional strain to promote promoter melting and DNA opening at lesion sites, whereas XPD acts as a 5' to 3' helicase responsible for lesion verification and extension of the repair bubble. Structural and biochemical studies have clarified how TFIIH subunits regulate these helicases-p52 and p8 modulate XPB's translocation activity, while p44, p62, and MAT1 control XPD's helicase function through conformational and compositional transitions within the complex. Beyond their canonical roles, XPB and XPD participate in diverse cellular pathways, including cell-cycle regulation and oxidative stress response, highlighting their involvement in maintaining genome integrity beyond repair and transcription. Mutations in either helicase lead to xeroderma pigmentosum (XP), trichothiodystrophy (TTD), or combined XP/Cockayne syndrome (XP/CS) phenotypes, emphasizing the essential role of TFIIH integrity for human health. Recent biochemical and pharmacological advances have further revealed the therapeutic relevance of these helicases-XPB as a target of small-molecule inhibitors such as triptolide, Minnelide, and spironolactone, and XPD as a potential modulator of cancer sensitivity to DNA-damaging treatments. Collectively, XPB and XPD exemplify the structural and functional versatility of TFIIH helicases across repair, transcription, and genome maintenance. - Source: PubMed
Publication date: 2026/03/13
Bravo MarcoFan Li - Sarcomatoid carcinoma of the bladder is a rare and aggressive biphasic malignant neoplasm, representing approximately 0.1-0.3% of all bladder cancers. It is characterized by the coexistence of malignant epithelial and mesenchymal components. Its poor prognosis and limited systemic treatment options underscore the need for improved molecular characterization. - Source: PubMed
Publication date: 2026/03/10
Morris GeorgeVlachostergios Panagiotis JRai Manoj PScherr DouglasMolina AnaElemento OlivierMosquera Juan MiguelCheng LiangFaltas Bishoy M - Cockayne syndrome is an ultra-rare (1:2.5 million) hereditary disease from the group of progeroid syndromes caused by pathogenic and probable-pathogenic variants in DNA repair genes (ERCC8, ERCC6, XPB (ERCC3), XPD (ERCC2) and XPG (ERCC5)) and characterized by abnormal photosensitivity, congenital cataract, microcephaly, sensorineural hearing loss, nervous system pathology and other multisystem changes. In this manuscript, for the first time in the Russian Federation, we present the results of a clinical and genetic study and follow-up of a Russian cohort of patients. - Source: PubMed
Publication date: 2026/03/07
Kungurtseva A LPopovich A VTikhonovich Yu VIvannikova T EKovalskaia V AVasiliev P AVitebskaya A V