ABCC2
- Known as:
- ABCC2
- Catalog number:
- 000908A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCC2
Related genes to: ABCC2
- Gene:
- ABCC2 NIH gene
- Name:
- ATP binding cassette subfamily C member 2
- Previous symbol:
- CMOAT
- Synonyms:
- DJS, MRP2, cMRP
- Chromosome:
- 10q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-09
- Date modifiied:
- 2019-04-23
Related products to: ABCC2
Related articles to: ABCC2
- To examine factors affecting the apparent clearance (CL/F) of total methotrexate polyglutamates (MTX-PGs) in red blood cells (RBCs) in Japanese patients with rheumatoid arthritis (RA) using population pharmacokinetic analysis. - Source: PubMed
Publication date: 2026/08/13
Hakamata JunKaneko YukoShimizu MikikoTakeuchi TsutomuHashiguchi Masayuki - Cancer pain affects more than half of all oncology patients and represents one of the most challenging therapeutic problems in modern medicine. Despite the central role of opioids in cancer pain management-codified by the WHO analgesic ladder-the clinical response to these agents is highly variable between individuals. Pharmacogenomics promises to explain this heterogeneity by identifying functionally relevant genetic polymorphisms in genes encoding opioid receptors, metabolizing enzymes, and membrane transport proteins. However, after two decades of intensive research, clinical translation of genetic data into actionable prescribing strategies remains elusive. A narrative-critical review of the literature was conducted by searching PubMed, Scopus, and Web of Science databases from inception to March 2026, using the search terms "opioid," "pharmacogenomics," "pharmacogenetics," "cancer pain," "polymorphism," and individual gene names (OPRM1, CYP2D6, COMT, ABCB1, SLC22A1, UGT2B7, and others). Reference lists of included articles were hand-searched for additional relevant studies. Inclusion was restricted to English-language articles reporting original data or systematic reviews on genetic polymorphisms and opioid response, with priority given to studies conducted in cancer pain populations. Clinical practice guidelines from CPIC, NCCN, ESMO, EAPC, and ASCO were consulted for current recommendations. This narrative-critical review examines the evidence on genetic polymorphisms relevant to opioid response in cancer pain, covering three functional categories: (1) pharmacodynamic genes, including opioid receptors (OPRM1, OPRD1, OPRK1) and neuromodulatory targets (COMT, KCNJ6, MC1R); (2) pharmacokinetic enzymes (CYP2D6, CYP3A4/5, UGT2B7); and (3) membrane transporters, including ABC efflux pumps (ABCB1, ABCG2, ABCC2) and SLC uptake carriers (SLC22A1, SLCO1B1, SLC6A4, SLC6A2). A dedicated section addresses the direct and indirect interference of the tumour itself-through the tumour microenvironment, neuroimmune signalling, epigenetic reprogramming, and cancer-induced organ dysfunction-on opioid pharmacogenomics. The overall evidence is poor and fragmented, a finding intrinsic to the extraordinary diversity, large number, and context-dependent biological activity of the polymorphisms identified. The tumour itself acts as a pervasive confounder that systematically distorts genotype-phenotype relationships. The path forward requires a paradigm shift from candidate-gene association studies to system pharmacogenomics and multi-omic integration. - Source: PubMed
Publication date: 2026/08/04
Mercadante Sebastiano - Salinity fluctuations pose critical physiological challenges to the sea cucumber Apostichopus japonicus. This review elucidated its molecular salinity response mechanisms, focusing on miRNA-mediated regulation and core pathways. We highlight a hierarchical network in which 8 key miRNAs fine-tune responses. let-7 targeted Solute Carrier Family 34 Member 2 (SLC34A2) and Cystathionine Gamma-Lyase (CTH), coordinating ion transport and amino acid metabolism, respectively. miR-10 targeted genes Nicotinamide Phosphoribosyltransferase (NAMPT) in energy homeostasis and TGF-Beta Activated Kinase 1 (MAP3K7) Binding Protein 1 (Table 1) to regulate MAPK/ERK signaling. miR-278-3p targeted 5-Hydroxytryptamine Receptor 2B (Htr2b) and Chloride Channel Accessory 1 (CLCA1) to modulate GPCR signaling and chloride transport. miR-2008, miR-3, miR-16, miR-22, and miR-14 coordinate vesicular trafficking, transcription, apoptosis, and autophagy via targeting Pleckstrin Homology Domain Containing A3 (PLEKHA3), Upstream Binding Transcription Factor (UBTF), ATP Binding Cassette Subfamily C Member 2 (ABCC2), Polypeptide N-Acetylgalactosaminyltransferase 2 (GALNT2), Glutamic-Oxaloacetic Transaminase 2 (Got2), Aconitase 2 (Aco2), and RNA Polymerase II Associated Protein 2 (Rpap2). Salinity sensing initiates GPCR-mediated cAMP/PKA and MAPK/ERK cascades, activating transcription factors (UBTF) to drive stress gene expression. Ion transporters (SLC family), ABC transporters, and vesicular transport maintain cellular homeostasis. Cullin Associated and Neddylation Dissociated 1 (CAND1)/Listerin E3 ubiquitin protein ligase 1 (Ltn1) are involved in amino acid/protein metabolism and ubiquitinated proteins to participate in vesicular transport for protein sorting and secreting. These secreted molecules (Glyare/Taurine) act as ligands to bind membrane receptors and trigger GPCR pathways and energy metabolism and redox balance. Aco2/Got2/NAMPT supply ATP for adaptation and apoptosis/autophagy, repair damage and maintain homeostasis, alleviate oxidative damage, supported by innate immunity genes. These findings establish a framework for understanding sea cucumbers salinity adaption, further exploration of additional genes is needed to refine mechanistic details. - Source: PubMed
Publication date: 2026/08/10
Chen JunweiZhao YudiLi NanWang HuiWu XuesongWang BaichangWei XinChang YaqingTian Yi - Dubin-Johnson Syndrome (DJS) is a rare inherited disorder characterized by isolated conjugated hyperbilirubinemia without significant liver damage. This syndrome is often diagnosed incidentally during routine blood tests, as it typically presents with minimal or no symptoms. The disease results from a genetic defect in the gene, which encodes the MRP2 protein responsible for transporting conjugated bilirubin out of hepatocytes. In individuals with DJS, the impaired function of MRP2 leads to the accumulation of conjugated bilirubin in the liver and bloodstream. This case report presents a 31-year-old female who, during pregnancy, developed icterus, which raised concerns about possible liver disease or viral hepatitis. However, further investigation revealed no significant liver dysfunction or risk factors for viral hepatitis. Laboratory tests showed elevated total and direct bilirubin levels, with normal liver enzymes, thus prompting further evaluation. Ultrasound imaging of the liver and biliary system revealed no signs of obstruction, and tests for viral hepatitis were negative. The patient's clinical history of icterus since childhood, combined with the laboratory findings, led to the suspicion of DJS. Notably, urine coproporphyrin analysis demonstrated a characteristic increase in coproporphyrin I, further supporting the diagnosis. Although DJS does not typically require treatment, the patient was provided with genetic counseling to inform her and her family about the condition and potential inheritance patterns. DJS presents a diagnostic challenge due to its subtle clinical features and the need to differentiate it from other causes of icterus, especially in pregnancy. This case highlights the importance of considering rare genetic disorders in the differential diagnosis of icterus and emphasizes the role of genetic testing in confirming the diagnosis. Early recognition of DJS allows for appropriate management and genetic counseling, ensuring that affected individuals can lead a normal life without major complications. - Source: PubMed
Publication date: 2026/08/06
Mousavi Said Reza ModaresPourhasan FarabSimab Pouria AhmadiBeikmohammadi-Gharehsaghghal SepidehKaini-Shamsabadi DaryoushKarimzadeh-Soureshjani Elaheh - Pharmacogenomic (PGx) variation is an important determinant of inter-individual variability in drug response. While germline pharmacogenomics has been extensively studied, somatic alterations affecting these pharmacogenes in tumors remain less systematically characterised. - Source: PubMed
Publication date: 2026/07/22
AlMulla AishaKaur SimerpreetBalyan PrachiAl-Saafin SanaBalyan Manoj KumarVelayutham DineshJithesh Puthen Veettil