scispace - formally typeset
S

Stephen P. Malkoski

Researcher at University of Colorado Denver

Publications -  23
Citations -  1094

Stephen P. Malkoski is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Cancer & Lung cancer. The author has an hindex of 12, co-authored 18 publications receiving 990 citations. Previous affiliations of Stephen P. Malkoski include University of New Mexico & Netherlands Cancer Institute.

Papers
More filters
Journal ArticleDOI

Composite Glucocorticoid Regulation at a Functionally Defined Negative Glucocorticoid Response Element of the Human Corticotropin-Releasing Hormone Gene

TL;DR: Results are consistent with a composite mechanism of glucocorticoid-dependent repression involving direct DNA binding of GR and AP-1 nucleoproteins at discrete adjacent sites within the CRH promoter.
Journal ArticleDOI

Smad4 loss in mice causes spontaneous head and neck cancer with increased genomic instability and inflammation

TL;DR: It is found that Smad4 was frequently downregulated not only in human head and neck squamous cell carcinoma (HNSCC) malignant lesions, but also in grossly normal adjacent buccal mucosa and severe inflammation was exhibited, which was associated with increased expression of TGF-beta1 and activated Smad3.
Journal ArticleDOI

Novel Stem/Progenitor Cell Population from Murine Tracheal Submucosal Gland Ducts with Multipotent Regenerative Potential

TL;DR: It is demonstrated that airway submucosal gland (SMG) duct cells, in addition to BCs, survived severe hypoxic‐ischemic injury and are therefore a multipotent stem cell for airway epithelial repair.
Journal ArticleDOI

Localization of a negative glucocorticoid response element of the human corticotropin releasing hormone gene.

TL;DR: It is concluded that (i) cAMP dependent activation of the CRH promoter is mediated primarily by the CRE at -224 bp, (ii) glucocorticoid-dependent repression is specific for theCRH promoter, and not a generalized effect of glucocortsicoid signaling or interference with the protein kinase A (PKA) signaling pathway.