Conditional inactivation of Akt three isoforms causes tau hyperphosphorylation in the brain

Molecular Neurodegeneration

Volumn 10, Issue 1, 2015, Pages

  Wang, Long ^a   Cheng, Shanshan ^a   Yin, Zhenyu ^b   Xu, Congyu ^a   Lu, Shuangshuang ^a   Hou, Jinxing ^a   Yu, Tingting ^b   Zhu, Xiaolei ^b   Zou, Xiaoyan ^a   Peng, Ying ^c   Xu, Yun ^b   Yang, Zhongzhou ^a   Chen, Guiquan ^a  

^a NANJING UNIVERSITY   (China)

^b MEDICAL SCHOOL OF NANJING UNIVERSITY   (China)

^c INSTITUTE OF MATERIA MEDICA   (China)

Author keywords

Akt; GSK3 and PKA; Tau kinases; Tau phosphorylation

Indexed keywords

BETA CATENIN; CYCLIC AMP DEPENDENT PROTEIN KINASE; GLYCOGEN SYNTHASE KINASE 3ALPHA; GLYCOGEN SYNTHASE KINASE 3BETA; MICROTUBULE ASSOCIATED PROTEIN 2; NEURON SPECIFIC NUCLEAR PROTEIN; PROTEIN KINASE B; TAU PROTEIN; AKT1 PROTEIN, MOUSE; AKT2 PROTEIN, MOUSE; AKT3 PROTEIN, MOUSE; GLYCOGEN SYNTHASE KINASE 3; ISOPROTEIN; MAPT PROTEIN, MOUSE; NERVE PROTEIN; TAMOXIFEN;

ARTICLE; CELL SURVIVAL; CEREBELLUM; CONTROLLED STUDY; CYTOPLASM; DEGENERATIVE DISEASE; DENTATE GYRUS; DOWN REGULATION; ENZYME INACTIVATION; GENE DELETION; HIPPOCAMPAL CA3 REGION; IMMUNOHISTOCHEMISTRY; IMMUNOREACTIVITY; LOXP SITE; MOUSE; NONHUMAN; PROTEIN FUNCTION; PROTEIN PHOSPHORYLATION; TUNEL ASSAY; WESTERN BLOTTING; ANIMAL; BIOSYNTHESIS; BRAIN; CROSS BREEDING; DEFICIENCY; DRUG EFFECTS; ENZYME INDUCTION; GENE EXPRESSION REGULATION; GENETICS; KNOCKOUT MOUSE; METABOLISM; PHOSPHORYLATION; PHYSIOLOGY; PROTEIN PROCESSING; SIGNAL TRANSDUCTION;

MUS;

ANIMALS; BRAIN; CROSSES, GENETIC; CYCLIC AMP-DEPENDENT PROTEIN KINASES; ENZYME INDUCTION; GENE EXPRESSION REGULATION; GLYCOGEN SYNTHASE KINASE 3; MAP KINASE SIGNALING SYSTEM; MICE; MICE, KNOCKOUT; NERVE TISSUE PROTEINS; PHOSPHORYLATION; PROTEIN ISOFORMS; PROTEIN PROCESSING, POST-TRANSLATIONAL; PROTO-ONCOGENE PROTEINS C-AKT; TAMOXIFEN; TAU PROTEINS;

EID: 84938326464     PISSN: None     EISSN: 17501326     Source Type: Journal    
DOI: 10.1186/s13024-015-0030-y     Document Type: Article

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