scispace - formally typeset
G

Glenn Longenecker

Researcher at National Institutes of Health

Publications -  19
Citations -  4688

Glenn Longenecker is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Cyclin-dependent kinase 5 & Ameloblast. The author has an hindex of 17, co-authored 19 publications receiving 4500 citations.

Papers
More filters
Journal ArticleDOI

Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death.

TL;DR: Cdk5(-/-) mice exhibit unique lesions in the central nervous system associated with perinatal mortality and also suggest that Cdk5 may play critical roles in neuronal cytoskeleton structure and organization.
Journal ArticleDOI

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.
Journal ArticleDOI

Adenovirus-mediated in vivo gene transfer and expression in normal rat liver.

TL;DR: Targeted gene expression has been achieved in the liver, albeit at low levels, suggesting that adenovirus vectors may be a useful means for in vivo gene therapy in liver disorders.
Journal ArticleDOI

Amelogenin-deficient mice display an amelogenesis imperfecta phenotype.

TL;DR: The disruption of the amelogenin locus is disrupted to generate amelgenin null mice, which display distinctly abnormal teeth as early as 2 weeks of age with chalky-white discoloration, and reveals that the amELogenins are apparently not required for initiation of mineral crystal formation but rather for the organization of crystal pattern and regulation of enamel thickness.
Journal ArticleDOI

Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing.

TL;DR: It is proposed that SLPI is a pivotal endogenous factor necessary for optimal wound healing in mice null for the gene encoding SLPI, which show impaired cutaneous wound healing with increased inflammation and elastase activity.