Regulated expression of differentiation-associated keratins in cultured epidermal cells detected by monospecific antibodies to unique peptides of mouse epidermal keratins

Roop, Dennis R.; Huitfeldt, Henrik S.; Kilkenny, Anne; Yuspa, Stuart H.

doi:10.1111/j.1432-0436.1987.tb00162.x

Cited by 175 publications

(102 citation statements)

References 40 publications

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“…K14 is detectable throughout most of the epidermis, as well as in hair follicles. K1 is normally expressed at an early stage during differentiation of the epidermis, routinely detected in the first suprabasal layer and occasionally in basal cells that have just withdrawn from the cell cycle (20). The expression of K1 was delayed in ML.⌬␤RII epidermis as compared with controls (data not shown), presumably due to expansion of the proliferative compartment.…”

Section: Ml⌬␤rii Transgenic Mice Exhibit a Hyperplastic͞mentioning

confidence: 85%

Expression of a dominant-negative type II transforming growth factor β (TGF-β) receptor in the epidermis of transgenic mice blocks TGF-β-mediated growth inhibition

Wang

Greenhalgh

Bickenbach

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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133

125

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To determine whether a functional type II receptor of transforming growth factor ␤ (TGF-␤) is required to mediate the growth inhibitory effect of TGF-␤ on the skin in vivo, we have generated transgenic mice that overexpress a dominant negative-type II TGF-␤ receptor (⌬␤RII) in the epidermis. The ⌬␤RII mice exhibited a thickened and wrinkled skin, and histologically the epidermis was markedly hyperplastic and hyperkeratotic. In vivo labeling with BrdUrd showed a 2.5-fold increase in the labeling index over controls, with labeled nuclei occurring in both basal and suprabasal cells of transgenic epidermis. In heterozygotes, this skin phenotype gradually diminished, and by 10-14 days after birth the transgenic mice were indistinguishable from their normal siblings. However, when F 1 mice were mated to homozygosity, perinatal lethality occurred due to the severe hyperkeratotic phenotype, which restricted movement. Cultured primary keratinocytes from ⌬␤RII mice also exhibited an increased rate of growth in comparison with nontransgenic controls, and were resistant to TGF-␤-induced growth inhibition. These data document the role of the type II TGF-␤ receptor in mediating TGF-␤-induced growth inhibition of the epidermis in vivo and in maintenance of epidermal homeostasis.

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Section: Ml⌬␤rii Transgenic Mice Exhibit a Hyperplastic͞mentioning

confidence: 85%

Expression of a dominant-negative type II transforming growth factor β (TGF-β) receptor in the epidermis of transgenic mice blocks TGF-β-mediated growth inhibition

Wang

Greenhalgh

Bickenbach

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

133

125

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“…The regulation of keratinocyte differentiation by extracellular stimuli has been studied primarily; studies include suspension culture, high Ca 2ϩ , FCS, 1␣-25-dihydroxyvitamin D 3 , 12-O-tetradecanoylphorbol-13-acetate (TPA), and ceramide (15,(22)(23)(24)(25)(26)(27). However, the intracellular signaling mechanisms of differentiation are poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis Signal-regulating Kinase 1 (ASK1) Is an Intracellular Inducer of Keratinocyte Differentiation

Sayama¹,

Hanakawa²,

Shirakata³

et al. 2001

Journal of Biological Chemistry

122

104

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reduced DNA synthesis, and cell cycle analysis verified the differentiation. p38 MAP kinase inhibitors, SB202190 and SB203580, abolished the induction of differentiation markers, transglutaminase-1, loricrin, and involucrin. In turn, the induction of differentiation with ceramide in keratinocytes caused an increase in ASK1 expression and activity. Furthermore, normal human skin expresses ASK1 protein in the upper epidermis, implicating ASK1 in in vivo keratinocyte differentiation. We propose that the ASK1-p38 MAP kinase cascade is a new intracellular regulator of keratinocyte differentiation.

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“…While this notion seems plausible, this simple model does not account for why there are two to three layers of cells with biochemical and morphological characteristics of basal cells in squamous cell carcinoma cells cultured on floating lattices of collagen and fibroblasts (Stoler et al, 1988;Kopan and Fuchs, 1989). Moreover, it does not explain why certain features of epidermal differentiation can be induced in basal cells before their exit from the innermost layer (Watt, 1984;Roop et al, 1987;Choi and Fuchs, 1990). Thus, it seems more likely that cessation of cell division can be uncoupled from loss of basement membrane contact and is key to when a cell shifts to a program of gene expression leading to terminal differentiation.…”

Section: Terminal Differentiation: Active or Passive?mentioning

confidence: 95%

“…Mouse keratinocytes seem to differ from human cells in their sensitivity to calcium. Recently, it was discovered that substantial K1/K10 expression in mouse epidermal cells can be induced by a narrow window of calcium concentrations (Roop et al, 1987;Yuspa et al, 1989). In addition, Glick et al (1990) showed that calcium induces a marked increase in TGF/T2 mRNA expression in mouse keratinocytes, thereby implicating calcium in both early and late stages of terminal differentiation.…”

Section: Calciummentioning

confidence: 99%

Epidermal differentiation: the bare essentials.

Fuchs

1990

The Journal of Cell Biology

609

481

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N the past ten years, there have been a number of major scientific discoveries in the field of epidermal differentiation. We owe many of these findings to the development of model tissue culture systems, and to technological advances in molecular biology. In this article, I will review some important aspects of the biology of terminal differentiation in vivo and in vitro, and highlight the recent advances in elucidating the molecular mechanism underlying these processes.

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Regulated expression of differentiation-associated keratins in cultured epidermal cells detected by monospecific antibodies to unique peptides of mouse epidermal keratins

Cited by 175 publications

References 40 publications

Expression of a dominant-negative type II transforming growth factor β (TGF-β) receptor in the epidermis of transgenic mice blocks TGF-β-mediated growth inhibition

Expression of a dominant-negative type II transforming growth factor β (TGF-β) receptor in the epidermis of transgenic mice blocks TGF-β-mediated growth inhibition

Apoptosis Signal-regulating Kinase 1 (ASK1) Is an Intracellular Inducer of Keratinocyte Differentiation

Epidermal differentiation: the bare essentials.

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