Ask about this productRelated genes to: SLC22A7 Blocking Peptide
- Gene:
- SLC22A7 NIH gene
- Name:
- solute carrier family 22 member 7
- Previous symbol:
- -
- Synonyms:
- NLT, OAT2
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-02-17
Related products to: SLC22A7 Blocking Peptide
Related articles to: SLC22A7 Blocking Peptide
- Kidney drug transporters, primarily located in the basolateral and apical membranes of proximal tubule cells, play a key role in the secretion and reabsorption of drugs and endogenous compounds. Recent studies have demonstrated that kidney diseases can alter transporter expression; however, the expression of these transporters in human transplanted kidneys, with and without rejection, remains unclear. Therefore, the aim of this study was to investigate the mRNA expression (qRT-PCR) and immunolocalization (via immunohistochemistry) of key ABC (ATP-binding cassette) (n = 14) and SLC (solute carriers) (n = 33) transporters in glomeruli and proximal tubule cells from human normal kidney (CTRL, n = 8), non-rejected transplanted kidney (AR-0, n = 7) and transplanted kidney under rejection process (AR-I, n = 8) from patients receiving immunosuppressive drugs. Our study shows that mRNA expression level of SLC22A4, SLC22A6, SLC22A7, SLC22A8, SLC28A1, SLC47A1, SLC22A11, SLC15A2, SLC16A1, ABCC2, ABCC5 and ABCC6 are statistically significantly downregulated, while SLC22A2, SLCO4A1 and ABCB1 are statistically upregulated in proximal tubule cells from rejected transplanted kidneys compared to controls. Immunohistochemistry revealed that OAT1, OAT3, OCT2, MATE1, MRP2, MRP6 and P-gp were primarily expressed in proximal tubule cells, with significantly lower protein expression of OAT1, OAT3, P-gp in AR-I and AR-0 biopsies compared to CTRL sections. These preliminary data suggest that the expression profile of kidney transporters may be altered in transplanted kidneys from patients treated with immunosuppressive drugs. - Source: PubMed
Publication date: 2026/01/23
Łapczuk-Romańska JHybiak JPiotrowska KMarchelek-Myśliwiec MWilk ASłojewski MUrasińska EDroździk M - Hyperoxaluria, including primary and secondary hyperoxaluria, induces renal tubular damage, interstitial inflammation. This study aimed to elucidate the molecular mechanisms underlying hyperoxaluria-induced kidney injury by integrating multi-omics analyses in a glyoxylate-induced mouse model, focusing on transcriptomic, proteomic, and metabolomic alterations. - Source: PubMed
Publication date: 2025/10/28
Zou BangyuShu MengLu ChaoyueJia YiyingZhang ShuweiZhang DongxiangYing ZhaoxinFang ZiyuPeng YonghanGao Xiaofeng - Diarrhea is primary adverse effect of capecitabine (Cap) causing treatment discontinuation. The aim of this study was to construct an early-warning model for predicting the Cap-induced diarrhea. - Source: PubMed
Publication date: 2025/06/07
Liu ZhijunQiu ShiXu YuanWang XinranSun JianguoCui LiliYe LiyaLiang ZhengyanGao ShouhongChen WanshengWang Zhipeng - The aim is of this study to identify genetic single nucleotide polymorphisms associated with cardiovascular (CV) toxicity in patients of oncohematological profile receiving antitumor immune chemotherapy. - Source: PubMed
Publication date: 2025/03/28
Gimatdinova GeliyaDanilova OlesyaDavydkin IgorMilyutkina YuliyaSustretov AlexeyGalati GiuseppeCavarretta ElenaPeruzzi MariangelaGermanova Olga - Impaired hepatic and renal function influence Alzheimer's disease (AD) progression; however, whether AD progression affects these important organ functions remains unclear. Here, we investigated the impact of AD progression, characterized by brain amyloid-beta (Aβ) accumulation, on liver and kidney function of App (APP-KI) mice using quantitative proteomics. SWATH-based quantitative proteomics revealed changes in mitochondrial, drug metabolism, and pharmacokinetic-related proteins in mouse liver and kidneys during the early (2-month-old) and intermediate (5-month-old) stages of Aβ accumulation. Notably, in 5-month-old APP-KI mouse liver, 25 phase I/II metabolizing enzymes (8 CYPs, 7 UGTs, 7 CESs, and 3 SLCs) and five transporters (2 ABCs and 3 SLCs) were significantly altered; specifically, Ugt1a9 and Slc33a1 protein abundances increased, whereas Ugt1a1 and Abcc3 protein abundances decreased. In the kidneys, 13 phase I/II metabolizing enzymes and 10 ABC-SLC transporters were altered, including Ugt1a6, Ugt1a7, Slc22a7, and Abcb1a. Additionally, plasma proteins, such as albumin and alpha-1-acid glycoprotein, which are critical for drug binding and distribution, were also altered. These results underscore the significant role of progressive brain Aβ accumulation in modifying hepatic and renal protein abundances, potentially influencing drug metabolism and disposition in AD. Our findings provide novel insights into the complex relationship between AD progression and organ dysfunction. - Source: PubMed
Publication date: 2024/11/01
Ito ShingoIwata YumiOtsuka MitsumiKaneko YuiOgata SeiryoYagi RyotaroUemura TatsukiMasuda TakeshiSaito TakashiSaido TakaomiOhtsuki Sumio