NAA10 controls osteoblast differentiation and bone formation as a feedback regulator of Runx2

Nature Communications

Volumn 5, Issue , 2014, Pages

  Yoon, Haejin ^a   Kim, Hye Lim ^a   Chun, Yang Sook ^a   Shin, Dong Hoon ^a   Lee, Kyoung Hwa ^a   Shin, Chan Soo ^a   Lee, Dong Yeon ^a   Kim, Hong Hee ^a   Lee, Zang Hee ^a   Ryoo, Hyun Mo ^a   Lee, Mi Ni ^b   Oh, Goo Taeg ^b   Park, Jong Wan ^a  

^a Seoul National University   (South Korea)

^b Ewha Womans University   (South Korea)

Author keywords

[No Author keywords available]

Indexed keywords

ACYLTRANSFERASE; BONE MORPHOGENETIC PROTEIN 2; N ALPHA ACYLTRANSFERASE 10; TRANSCRIPTION FACTOR RUNX2; UNCLASSIFIED DRUG; N-ALPHA-ACETYLTRANSFERASE 10, RAT; NAA10 PROTEIN, MOUSE; PEPTIDE ALPHA N ACETYLTRANSFERASE; PEPTIDE ALPHA N ACETYLTRANSFERASE A; PEPTIDE ALPHA N ACETYLTRANSFERASE E; RUNX2 PROTEIN, MOUSE; RUNX2 PROTEIN, RAT;

DEVELOPMENTAL BIOLOGY; ENZYME ACTIVITY; GENE; GENETIC DIFFERENTIATION; INHIBITION; RODENT; SIGNALING; STABILIZATION;

ADULT; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BONE REGENERATION; CELL DIFFERENTIATION; CONTROLLED STUDY; FEEDBACK SYSTEM; FEMALE; FRACTURE HEALING; GENETIC TRANSCRIPTION; MALE; MOUSE; NEWBORN; NONHUMAN; OSSIFICATION; OSTEOBLAST; PROTEIN ACETYLATION; PROTEIN BINDING; PROTEIN FUNCTION; PROTEIN STABILITY; RAT; SIGNAL TRANSDUCTION; SKULL DEFECT; TRANSCRIPTION REGULATION; AMINO ACID SEQUENCE; ANIMAL; BONE DEVELOPMENT; CELL CULTURE; CYTOLOGY; DEFICIENCY; GENETICS; INJURIES; KNOCKOUT MOUSE; MOLECULAR GENETICS; PHYSIOLOGY; SKULL; SPRAGUE DAWLEY RAT; TRANSGENIC MOUSE; WOUND HEALING;

MAMMALIA; MUS; RATTUS;

AMINO ACID SEQUENCE; ANIMALS; BONE REGENERATION; CELL DIFFERENTIATION; CELLS, CULTURED; CORE BINDING FACTOR ALPHA 1 SUBUNIT; FEEDBACK, PHYSIOLOGICAL; FEMALE; MALE; MICE; MICE, KNOCKOUT; MICE, TRANSGENIC; MOLECULAR SEQUENCE DATA; N-TERMINAL ACETYLTRANSFERASE A; N-TERMINAL ACETYLTRANSFERASE E; N-TERMINAL ACETYLTRANSFERASES; OSTEOBLASTS; OSTEOGENESIS; RATS; RATS, SPRAGUE-DAWLEY; SIGNAL TRANSDUCTION; SKULL; WOUND HEALING;

EID: 84923355497     PISSN: None     EISSN: 20411723     Source Type: Journal    
DOI: 10.1038/ncomms6176     Document Type: Article

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