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Below is a list of our research faculty and a brief
description of their interests. Click on the name of the researcher to
view their web page.
My group has an interest in understanding the skin pigmentary system and the potential role of melanocyte stem cells in hyperpigmentation and in pigmentation diseases such as vitiligo or premature graying where melanocyte loss is observed. We are focused on finding effective therapies for these conditions.
The goal of our laboratory is to elucidate the role of desmosomal genes
and proteins in the normal development of the skin and its appendages
(hair follicles, mammary glands). Furthermore, we are investigating how
mutations in desmosomal genes lead to diseases (skin fragility
disorders, skin cancer). To accomplish these goals, we are generating
and characterizing genetically engineered mice which either lack
expression of certain desmosomal genes (knockout mice) or which express
mutant versions of these genes (transgenic mice, knockin mice). In order
to understand how desmosomal genes are regulated during embryonic
development of the skin and its appendages, we are also analyzing the
role of epidermal signal transduction pathways (e.g. Wnt and NFкB) in
regulating the expression of the desmosomal genes.
My research is aimed at identifying the signaling pathways that control
epidermal development and differentiation. A key regulator of epidermal
development is p63, a transcription factor that is expressed as six
different isoforms. Mice lacking all p63 isoforms do not develop an
epidermis or skin appendages, such as hair follicles and mammary
glands. Using genetically engineered mice, my laboratory studies the
role of p63 isoforms during embryonic development and postnatal
differentiation of the skin. In addition, p63 is mutated in a subset of
ectodermal dysplasias, inherited disorders that are characterized by
abnormalities of the skin and skin appendages. One of our other research
objectives is to use mouse models to identify the pathogenic mechanisms
that underlie skin fragility in patients with these disorders.
Our laboratory is interested in defining the molecular mechanisms
involved in the initiation, establishment and maintenance of lymphoid
tumors. We have based our work on the hypothesis that lymphoid neoplasms
arise as a result of the dysregulation of signals that normally control
lymphoid function and homeostasis.
My research focuses on understanding the role of cancer stem cells in the maintenance and resistance of skin cancer. We are developing stem cell therapies for inherited skin blistering diseases. We are also developing stem cell therapies for wound repair.
My research is focused on the mechanisms involved in melanoma
chemoresistance and to develop methods to reverse the resistance of
melanoma to therapy. My goal is to determine the mechanisms through which survivin functions
in melanoma and whether survivin expression is associated with
progression of melanoma.
Transcriptional regulation governs a broad
spectrum of cellular activities: cell cycle progression, cell migration,
apoptosis, or metabolism. We are interested in elucidating the
molecular mechanisms underlying transcriptional regulation in response
to physiological and pathological signals.
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