Aminoaciduria, but normal thyroid hormone levels and signaling, in mice lacking the amino acid and thyroid hormone transporter Slc7a8

التفاصيل البيبلوغرافية
العنوان: Aminoaciduria, but normal thyroid hormone levels and signaling, in mice lacking the amino acid and thyroid hormone transporter Slc7a8
المؤلفون: Eva K. Wirth, Marc Klein, Annette Grüters, Ulrich Schweizer, Doreen Braun, Franziska Wohlgemuth, Nathalie Reix, Josef Köhrle
المساهمون: Institut fur Experimentelle Endokrinologie, Charité - UniversitätsMedizin = Charité - University Hospital [Berlin]
المصدر: Biochemical Journal
Biochemical Journal, Portland Press, 2011, 439 (2), pp.249-255. ⟨10.1042/BJ20110759⟩
بيانات النشر: HAL CCSD, 2011.
سنة النشر: 2011
مصطلحات موضوعية: Thyroid Hormones, medicine.medical_specialty, Amino Acid Transport System y+, Blotting, Western, Biology, Polymerase Chain Reaction, Biochemistry, Mice, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Neutral amino acid transport, medicine, Animals, Amino acid transporter, Amino Acid Metabolism, Inborn Errors, Molecular Biology, DNA Primers, 030304 developmental biology, Mice, Knockout, chemistry.chemical_classification, Monocarboxylate transporter, 0303 health sciences, Base Sequence, Fusion Regulatory Protein 1, Light Chains, Thyroid, Brain, Life Sciences, Transporter, Cell Biology, medicine.disease, Immunohistochemistry, Amino acid, Mice, Inbred C57BL, Endocrinology, medicine.anatomical_structure, chemistry, Aminoaciduria, biology.protein, 030217 neurology & neurosurgery, Signal Transduction, Hormone
الوصف: LAT2 (system L amino acid transporter 2) is composed of the subunits Slc7a8/Lat2 and Slc3a2/4F2hc. This transporter is highly expressed along the basolateral membranes of absorptive epithelia in kidney and small intestine, but is also abundant in the brain. Lat2 is an energy-independent exchanger of neutral amino acids, and was shown to transport thyroid hormones. We report in the present paper that targeted inactivation of Slc7a8 leads to increased urinary loss of small neutral amino acids. Development and growth of Slc7a8−/− mice appears normal, suggesting functional compensation of neutral amino acid transport by alternative transporters in kidney, intestine and placenta. Movement co-ordination is slightly impaired in mutant mice, although cerebellar development and structure remained inconspicuous. Circulating thyroid hormones, thyrotropin and thyroid hormone-responsive genes remained unchanged in Slc7a8−/− mice, possibly because of functional compensation by the thyroid hormone transporter Mct8 (monocarboxylate transporter 8), which is co-expressed in many cell types. The reason for the mild neurological phenotype remains unresolved.
اللغة: English
تدمد: 0264-6021
1470-8728
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3a7ac0bddd6a4b0a4f4db15785bcee5aTest
https://hal.archives-ouvertes.fr/hal-00628667/file/PEER_stage2_10.1042%2FBJ20110759.pdfTest
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....3a7ac0bddd6a4b0a4f4db15785bcee5a
قاعدة البيانات: OpenAIRE