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Validated All-in-One™ qPCR Primer for SLC22A1(NM_003057.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
Polyspecific organic cation transporters in the liver, kidney, intestine, and other organs are critical for elimination of many endogenous small organic cations as well as a wide array of drugs and environmental toxins. This gene is one of three similar cation transporter genes located in a cluster on chromosome 6. The encoded protein contains twelve putative transmembrane domains and is a plasma integral membrane protein. Two transcript variants encoding two different isoforms have been found for this gene, but only the longer variant encodes a functional transporter. [provided by RefSeq].
Gene References into function
- investigation of polymorphisms affecting function
- identification of genetic variations and their functional consequences
- Selective inhibition of class switching to IGG and IgE by recruitment of this and HOXC4 proteins and Ku70/ku86 to newly identified ATTT cis-elements.
- Evolutionary conserved amino acids predict the function of variants of this protein.
- identification of single nucleotide polymorphisms of organic cation transporter 1 (SLC22A1) affecting transport functions
- organic cation transporter EMT mRNA was mainly detected in the intra lobular septa and together with organic cation transporters OCT1 and OCT2 mRNAs also expressed in scattered cells of placental vessel adventitias
- hOCT1 was inhibited by PKA and endogenously activated by calmodulin, calmodulin-dependent kinase II, and p56(lck) tyrosine kinase
- Twenty genetic variations, including seven novel ones, have been found in the human SLC22A1 gene from 116 Japanese individuals.
- OCT1 and OCT2 mediate luminal ACh release in human airways
- Ranitidine and famotidine elicited differential inhibitory activities on SLC22A1.
- findings suggest that genetic variants of hOCTs are not linked among three genes in a Korean population, and several of the hOCT genetic variants cause decreased transport activity in vitro compared with the wild type
- Genetic variation in OCT1 may be associated with variation in response to metformin.
- Cholesterol treatment led to increased levels of NTCP and OCT-1 mRNAs.
- These results suggest that the saturable component in the hepatic uptake of these cationic compounds may be mediated mainly by hOCT1/rOct1.
- P-gp, rather than BCRP or OCT1, is partially responsible for the development of imatinib-resistance due to constitutive and functional overexpression, leading to reduced intracellular accumulation of imatinib in resistant K562 cells.
- Varenicline was characterized as a moderate-affinity substrate for hOCT2 (K(m)=370 microM) and its hOCT2-mediated uptake was partially inhibited by cimetidine.
- SLC22A1 expression is a composite surrogate for expression of various transporters relevant to imatinib intracellular uptake and retention
- Unlike imatinib, dasatinib cellular uptake is not significantly affected by OCT-1 activity, so that expression and function of OCT-1 is unlikely to affect response to dasatinib.
- hOCT1 is not required for dasatinib uptake in human cells
