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Sergey Leikin
Researcher at National Institutes of Health
Publications - 96
Citations - 7562
Sergey Leikin is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Type I collagen & Osteogenesis imperfecta. The author has an hindex of 45, co-authored 92 publications receiving 6109 citations. Previous affiliations of Sergey Leikin include University of Maryland, Baltimore & Russian Academy of Sciences.
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Haploinsufficiency for either one of the type-II regulatory subunits of protein kinase A improves the bone phenotype of Prkar1a+/− mice
Sisi Liu,Emmanouil Saloustros,Edward L. Mertz,Kit Man Tsang,Matthew F. Starost,Paraskevi Salpea,Fabio R. Faucz,Eva Szarek,Maria Nesterova,Sergey Leikin,Constantine A. Stratakis +10 more
TL;DR: Haploinsufficiency for either of PKA-II regulatory subunits improved bone phenotype of mice haploinsufficient for Prkar1a, in support of the hypothesis that the PRKAR2A and PRKar2B regulatory subunit were in part responsible for the bone phenotypeof Prkar 1a(+/-) mice.
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Erratum: ``Theory of interaction between helical molecules'' [J. Chem. Phys. 107, 3656 (1997)]
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Chain-melting reentrant transition in bimolecular layers at large separations.
TL;DR: A reentrant phase transition within well-separated bimolecular layers of diacylphosphates is detected and the disorder-order-disorder transitions of the hydrocarbon chains can be accounted for on the basis of the electrostatic energy between bilayers and the elastic compressibility energy within bilayers.
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Celecoxib treatment of fibrous dysplasia (FD) in a human FD cell line and FD-like lesions in mice with protein kinase A (PKA) defects.
Emmanouil Saloustros,Sisi Liu,Edward L. Mertz,Nisan Bhattacharyya,Matthew F. Starost,Paraskevi Salpea,Maria Nesterova,Michael A. Collins,Sergey Leikin,Constantine A. Stratakis +9 more
TL;DR: Celecoxib had an inhibitory effect on FD cell proliferation and in mouse FDLL structure, respectively, and it is speculated that COX-2 inhibitors offer an attractive alternative to current treatments for benign tumors such as OMX and FD that may mechanically stabilize affected bones.
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Correction: Corrigendum: Prolyl 3-hydroxylase 1 deficiency causes a recessive metabolic bone disorder resembling lethal/severe osteogenesis imperfecta
Wayne A. Cabral,Weizhong Chang,Aileen M. Barnes,MaryAnn Weis,Melissa A Scott,Sergey Leikin,Elena Makareeva,Natalia V. Kuznetsova,Kenneth N. Rosenbaum,Cynthia J. Tifft,Dorothy I. Bulas,Chahira Kozma,Peter A. Smith,David R. Eyre,Joan C. Marini +14 more
TL;DR: In the version of this article initially published, the nucleotide positions of the mutations in the LEPRE1 cDNA and genomic DNA sequence in Table 1, Supplementary Table 1 and Supplementary Figure 1 were incorrectly numbered relative to the first nucleotide of exon 1 rather than the firstucleotide of the L EPRE1 start codon.