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Beatrice Sommer

Researcher at National Institutes of Health

Publications -  5
Citations -  1110

Beatrice Sommer is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Biglycan & Enhancer. The author has an hindex of 5, co-authored 5 publications receiving 1059 citations.

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Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice

TL;DR: This is the first report in which deficiency of a non-collagenous ECM protein leads to a skeletal phenotype that is marked by low bone mass that becomes more obvious with age and may serve as an animal model to study the role of ECM proteins in osteoporosis.
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Phenotypic effects of biglycan deficiency are linked to collagen fibril abnormalities, are synergized by decorin deficiency, and mimic Ehlers-Danlos-like changes in bone and other connective tissues.

TL;DR: It is reported that bgn deficiency leads to structural abnormality in collagen fibrils in bone, dermis, and tendon, and to a “subclinical” cutaneous phenotype with thinning of the dermis but without overt skin fragility.
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Differential display of human marrow stromal cells reveals unique mRNA expression patterns in response to dexamethasone

TL;DR: Differential display of DEX‐treated hBMSC revealed unique patterns of gene expression and has provided new information about phenotypic changes that accompany the differentiation of hB MSC toward osteogenesis.
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Efficient Gene Transfer into Normal Human Skeletal Cells Using Recombinant Adenovirus and Conjugated Adenovirus-DNA Complexes

TL;DR: Very efficient gene transfer into multilayered HMSF and HTB cell cultures was observed, and DNA coincubated with unmodified ADV failed to be effectively transferred, implying that the covalently bound PLL more effectively binds exogenous DNA, resulting in a highly efficient internalization event in both cell types.
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Transcriptional regulation restricting bone sialoprotein gene expression to both hypertrophic chondrocytes and osteoblasts.

TL;DR: This study identifies an important cis‐acting element in the BSP promoter that acts as a tissue‐specific enhancer of BSP expression in both osteoblasts and hypertrophic chondrocytes and is the first demonstration of a common regulatory mechanism utilized by both chondrobasts and osteoblast for the tissue‐restricted expression of the B SP gene.