Myeloid adrenergic signaling via CaMKII forms a feedforward loop of catecholamine biosynthesis

Author:

Luo Yan12,Liu Bilian1,Yang Xin2,Ma Xiaoxiao3,Zhang Xing24,Bragin Denis E5,Yang Xuexian O4,Huang Wendong3,Liu Meilian12

Affiliation:

1. Department of Endocrinology and Metabolism, Metabolic Syndrome Research Center, Key Laboratory of Diabetes Immunology, National Clinical Research Center for Metabolic Diseases, The Second Xiangya Hospital, Central South University, Changsha, China

2. Department of Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM, USA

3. Department of Diabetes Complications & Metabolism Research, City of Hope, Duarte, CA, USA

4. Department of Microbiology and Molecular Genetics, University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM, USA

5. Department of Neurosurgery, University of New Mexico Health Sciences Center School of Medicine, Albuquerque, NM, USA

Funder

National Institutes of Health

National Institute of Diabetes and Digestive and Kidney Diseases

R01 Award

NIDDK

American Diabetes Association

American Heart Association

University of New Mexico Health Sciences Center (UNMHSC)

AHA

RMSE

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Genetics,Molecular Biology,General Medicine

Reference39 articles.

1. Tyrosine hydroxylase. Activation by protein phosphorylation and end product inhibition;Ames;J. Biol. Chem.,1978

2. Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity;Brestoff;Nature,2015

3. Catecholamines in a macrophage cell line;Brown;J. Neuroimmunol.,2003

4. Regulation of tyrosine hydroxylase gene expression by the m1 muscarinic acetylcholine receptor in rat pheochromocytoma cells;Chen;Brain Res. Mol. Brain Res.,1996

5. Tyrosine hydroxylase and regulation of dopamine synthesis;Daubner;Arch. Biochem. Biophys.,2011

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