Human Polyclonal ERCC1 Ab
- Known as:
- Human Polyclonal ERCC1 Antibody
- Catalog number:
- a0777
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal ERCC1
Related genes to: Human Polyclonal ERCC1 Ab
- Gene:
- ERCC1 NIH gene
- Name:
- ERCC excision repair 1, endonuclease non-catalytic subunit
- Previous symbol:
- -
- Synonyms:
- RAD10
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-05-23
Related products to: Human Polyclonal ERCC1 Ab
Related articles to: Human Polyclonal ERCC1 Ab
- Understanding age-related changes in migraine is pivotal, considering the increasing global life expectancy. In addition, both aging and migraine are prominent cardiovascular risk factors. It remains unclear whether calcitonin gene-related peptide (CGRP) release changes with age across trigeminovascular components, and how this relates to peripheral responses to migraine-related vasodilatory molecules. The primary aim was to investigate age-related effects on CGRP release from the trigeminovascular system by studying a mouse model of combined accelerated neuronal and vascular aging, the DNA repair-deficient Ercc1 mice. Second, we assessed the effects of aging on isolated coronary vasodilatory responses to CGRP and forskolin. - Source: PubMed
Publication date: 2026/07/03
Al-Hassany LindaRubio-Beltrán EloisaLabastida-Ramirez AlejandroGarrelds Ingrid MDanser A H JanRoks Anton J MMaassenVanDenBrink Antoinette - Lung cancer is the primary cause of cancer deaths in the UK and globally, and the main subtypes are non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Many treatment options are available, with platinum-based chemotherapy being a key component for many patients. However, variation in survival outcomes exists among individuals of European ancestry, which makes it important to identify germline genetic variants that help guide decision-making and optimise patient treatment and outcomes. - Source: PubMed
Publication date: 2026/06/24
Al-Matrafi Abdullah RBaxter Mark APearson Ewan RPetty Russell D - Prior studies have shown that cyclin D1 regulates diverse aspects of liver metabolism during cell cycle progression. Interestingly, this protein is induced in hepatocytes by feeding, but its function in modulating hepatic postprandial physiology is poorly characterized. The aim of this study was to evaluate the contribution of cyclin D1 to the hepatic response to feeding and to gain insight into its potential non-proliferative roles in other conditions. - Source: PubMed
Publication date: 2026/05/28
Wu HengHauser Jonathan IYang NaTimchenko NikolaiKlaers MaggieSalekeen RahagirManivel Juan CAbrahante Juan ELaux LinshanYousefzadeh Matthew JSchonfeld Michael PTikhanovich IrinaIkramuddin SayeedMonga Satdarshan SAdeyi Oyedele ANiedernhofer Laura JSen PayelGill Matthew SAlbrecht Jeffrey H - SLX4 is a scaffold protein pivotal in genome protection mechanisms ranging from homologous recombination and interstrand cross-link (ICL) repair to mechanisms that deal with challenged DNA replication. Many of human SLX4 functions rely on its ability to interact and control the XPF-ERCC1, MUS81-EME1, and SLX1 structure-specific endonucleases. Interaction with MUS81 relies on the conserved SAP domain of SLX4. Since the same domain in yeast Slx4 orthologs does not interact with Mus81, we investigated whether human SLX4 SAP might have retained some ancestral MUS81-independent functions. We show that human SLX4 SAP binds DNA with a preference for branched structures such as Holliday junctions. We further discovered that phosphorylation of SLX4 SAP by CDK1, which promotes interaction with MUS81, inhibits DNA binding. We identified separation of function mutants that impair either DNA or MUS81 binding. Binding to MUS81 is required in response to ICL-inducing agents, methyl methanesulfonate (MMS), TOP1, and PARP inhibition. Instead, DNA binding is required in response to ICL-inducing agents and MMS but not after TOP1 or PARP inhibition. Our work indicates that phosphorylation by CDK1 acts as a regulatory switch between DNA binding and MUS81-dependent functions of SLX4, to accommodate specific DNA lesions or secondary structures. - Source: PubMed
Scaglione SarahGaillard Pierre-Henri - Despite the adoption of neoadjuvant FLOT chemotherapy as standard treatment for locally advanced gastric and gastroesophageal junction cancer, many patients fail to achieve meaningful pathological response, limiting efficacy. The aim of this study was to evaluate the impact of pharmacogenetic markers on pathological response in Russian patients receiving neoadjuvant FLOT. Thirty patients with locally advanced gastric or gastroesophageal junction adenocarcinoma received neoadjuvant FLOT followed by surgery. Polymorphisms in (rs776746), (rs10509681, rs11572080, rs1058930), (rs11615), and (rs1695) were analyzed. Favorable pathological response (TRG0-2) was observed in 23.3% of patients, including 3.3% complete responses. Most patients (76.7%) had minimal or no regression (TRG3-5). Clinical variables were not associated with response. (rs11615) showed a significant association: patients with the Wt/Wt genotype had higher odds of achieving TRG0-2 (OR = 8.889; = 0.033; 95% CI: 1.294-61.058). No associations were found for , or . Median PFS was 18.21 months in TRG3-5, while not reached in TRG0-2 ( = 0.108). No significant PFS differences by genotype were observed ( = 0.525). (rs11615) may serve as a potential pharmacogenetic marker of response to FLOT, supporting further research in personalized treatment strategies. - Source: PubMed
Publication date: 2026/05/04
Fedorinov DenisLyadov VladimirLyadova MarinaAbdullaev SherzodKachanova AnastasiaFilatova AnnaIvashchenko DmitriySychev Dmitry