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p63 is a p53 homologue required for limb and epidermal morphogenesis
P63 is essential for several aspects of ectodermal differentiation during embryogenesis, including hair follicles, teeth and mammary glands, which are absent in p63-deficient mice.
p63 is the molecular switch for initiation of an epithelial stratification program.
The data demonstrate that p63 plays a dual role: initiating epithelial stratification during development and maintaining proliferative potential of basal keratinocytes in mature epidermis.
Keap1-null mutation leads to postnatal lethality due to constitutive Nrf2 activation
These experiments show that Keap1 acts upstream of Nrf2 in the cellular response to oxidative and xenobiotic stress, and breeding to NRF2-deficient mice reversed the phenotypic Keap 1 deficiencies.
Multiple defects and perinatal death in mice deficient in follistatin
Follistatin-deficient mice are retarded in then* growth, have decreased mass of the diaphragm and intercostal muscles, shiny taut skin, skeletal defects of the hard palate and the thirteenth pair of ribs, their whisker and tooth development is abnormal, they fail to breathe, and die within hours of birth, indicating that follistatin may modulate the actions of several members of the transforming growth factor-β family.
Functional analysis of activins during mammalian development
Mice lacking both activin subunits show the defects of both individual mutants but no additional defects, indicating that there is no functional redundancy between these proteins during embryogenesis.
Expression of murine epidermal differentiation markers is tightly regulated by restricted extracellular calcium concentrations in vitro
In vitro results suggest that the Ca2+ environment is a fundamental regulator of expression of epidermal differentiation markers and provide an explanation for the existence of theCa2+ gradient in vivo.
Cross-regulation between Notch and p63 in keratinocyte commitment to differentiation.
A complex cross-talk between Notch and p63 is involved in the balance between keratinocyte self-renewal and differentiation, with the Hes-1 gene as one of its direct negative targets.
Deregulated expression of c-Myc depletes epidermal stem cells
- R. Waikel, Y. Kawachi, Patricia A. Waikel, Xiao-Jing Wang, D. Roop
- Biology, MedicineNature Genetics
- 1 June 2001
It is concluded that deregulated expression of c-Myc in stem cells reduces β1 integrin expression, which is essential to both keratinocyte migration and stem cell maintenance.
Mechanisms regulating epithelial stratification.
- M. Koster, D. Roop
- Biology, Environmental ScienceAnnual Review of Cell and Developmental Biology
- 18 October 2007
This review summarizes the current advances that have been made in understanding the molecular mechanisms that regulate epidermal morphogenesis and outlines the priorities for further research.
Apoptotic Cells Activate the “Phoenix Rising” Pathway to Promote Wound Healing and Tissue Regeneration
The authors dub the molecular events associated with death-induced proliferation the “phoenix rising” pathway, which involves the caspase-mediated activation of phospholipase A2 and the subsequent production and release of the lipid signal prostaglandin E2, a stimulator of cell proliferation.