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huURAT1
製品ID :
C001704
系統:
C57BL/6NCya
状況:
説明:
The solute carrier family 22 member 12 gene ( SLC22A12) encodes the Urate Transporter 1 (URAT1), a critical transmembrane protein localized to the apical membrane of renal proximal tubule epithelial cells [1]. As the primary mediator of urate reabsorption from the glomerular filtrate, URAT1 plays a pivotal role in maintaining systemic urate homeostasis, a process essential for preventing hyperuricemia and its associated pathologies [2]. Genetic studies have identified numerous variants within SLC22A12 that are strongly linked to renal hypouricemia, characterized by impaired urate reabsorption and an increased risk of exercise-induced acute kidney injury [3]. Furthermore, polymorphisms in SLC22A12 influence the efficacy of uricosuric agents, highlighting its clinical relevance in the management of gout, a common inflammatory arthritis resulting from urate crystal deposition [4]. The functional importance of URAT1 underscores SLC22A12 as a key genetic determinant of urate metabolism and a significant factor in kidney health and disease.
huURAT1 mice are humanized models in which the sequences from upstream of exon 1 to exon 10 of the mouse Slc22a12 gene were replaced with the sequences from upstream of exon 1 to exon 10 of the human SLC22A12 gene. This model can be used to study the pathological mechanisms and therapeutic methods of renal hypouricemia, gout, and other uric acid metabolism-related diseases, as well as the screening and development of URAT1-targeted drugs, and preclinical efficacy and safety evaluations.
The solute carrier family 22 member 12 gene ( SLC22A12) encodes the Urate Transporter 1 (URAT1), a critical transmembrane protein localized to the apical membrane of renal proximal tubule epithelial cells [1]. As the primary mediator of urate reabsorption from the glomerular filtrate, URAT1 plays a pivotal role in maintaining systemic urate homeostasis, a process essential for preventing hyperuricemia and its associated pathologies [2]. Genetic studies have identified numerous variants within SLC22A12 that are strongly linked to renal hypouricemia, characterized by impaired urate reabsorption and an increased risk of exercise-induced acute kidney injury [3]. Furthermore, polymorphisms in SLC22A12 influence the efficacy of uricosuric agents, highlighting its clinical relevance in the management of gout, a common inflammatory arthritis resulting from urate crystal deposition [4]. The functional importance of URAT1 underscores SLC22A12 as a key genetic determinant of urate metabolism and a significant factor in kidney health and disease.
huURAT1 mice are humanized models in which the sequences from upstream of exon 1 to exon 10 of the mouse Slc22a12 gene were replaced with the sequences from upstream of exon 1 to exon 10 of the human SLC22A12 gene. This model can be used to study the pathological mechanisms and therapeutic methods of renal hypouricemia, gout, and other uric acid metabolism-related diseases, as well as the screening and development of URAT1-targeted drugs, and preclinical efficacy and safety evaluations.
B6-Uox KO/huURAT1
製品ID :
C001937
系統:
C57BL/6Cya
状況:
説明:
B6-Uox KO/huURAT1 mice are humanized disease models obtained by crossing Uox KO mice (catalog No.: C001232) with B6-huURAT1 mice (catalog No.: C001704). This model can be used for studying the pathological mechanisms and treatment methods of uric acid metabolism-related diseases such as hyperuricemia and gout, as well as for screening and developing URAT1-targeted therapies and evaluating preclinical efficacy and safety. It is worth noting that heterozygous Uox KO mice can survive and are fertile, while homozygous Uox KO mice need to be maintained with drugs such as Allopurinol after birth.
B6-Uox KO/huURAT1 mice are humanized disease models obtained by crossing Uox KO mice (catalog No.: C001232) with B6-huURAT1 mice (catalog No.: C001704). This model can be used for studying the pathological mechanisms and treatment methods of uric acid metabolism-related diseases such as hyperuricemia and gout, as well as for screening and developing URAT1-targeted therapies and evaluating preclinical efficacy and safety. It is worth noting that heterozygous Uox KO mice can survive and are fertile, while homozygous Uox KO mice need to be maintained with drugs such as Allopurinol after birth.
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