Sox21 deletion in mice causes postnatal growth deficiency without physiological disruption of hypothalamic-pituitary endocrine axes.

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作者： Leonard Y M,Cheung ^[1] ; Hideyuki,Okano ^[2] ; Sally A,Camper ^[3]

作者单位： Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA. ^[1] Department of Physiology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. ^[2] Department of Human Genetics, University of Michigan, Ann Arbor, MI, USA. Electronic address: scamper@med.umich.edu. ^[3]

关键词 Hypothalamus Metabolism Pituitary SOX21 SoxB1

主题词动物(Animals);动物, 新生(Animals, Newborn);基础代谢(Basal Metabolism);体重(Body Weight);间脑(Diencephalon);女(雌)性(Female);基因缺失(Gene Deletion);生长激素(Growth Hormone);生长和发育(Growth and Development);下丘脑(Hypothalamus);男(雄)性(Male);小鼠, 基因敲除(Mice, Knockout);器官特异性(Organ Specificity);垂体(Pituitary Gland);SOXB2转录因子类(SOXB2 Transcription Factors);甲状腺素(Thyroxine)

DOI 10.1016/j.mce.2016.09.005

PMID 27616671

发布时间 2018-11-13

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Molecular and cellular endocrinology

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213-223页

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Sox21 deletion in mice causes postnatal growth deficiency without physiological disruption of hypothalamic-pituitary endocrine axes.

Molecular and cellular endocrinology

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Molecular and cellular endocrinology

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Sox21 deletion in mice causes postnatal growth deficiency without physiological disruption of hypothalamic-pituitary endocrine axes.

Molecular and cellular endocrinology

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Molecular and cellular endocrinology

相关期刊

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