c-jun and junB antagonistically control cytokine-regulated mesenchymal-epidermal interaction in skin

Article Abstract:

Results show that in keratinocyte proliferation and differentiation, transcription factor AP-1 antagonistically control as seen in skin reconstitution experiments employing human keratinocytes and mouse c-jun and junB fibroblasts.

Physiological aspects, Keratinocytes, Cytokines, Homeostasis

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Chronic myeloid leukemia with increased granulocyte progenitors in mice lacking JunB expression in the myeloid lineage

Article Abstract:

Research demonstrates that JunB gene is a key transcriptional regulator of myelopoiesis as evidenced by the development of myeloproliferative diseases in the absence of the gene. Data further suggest that JunB is a potential tumor suppressor gene.

Statistical Data Included, Analysis, Abnormalities, Gene expression, Tumor suppressor genes, Granulocytes, Myeloblastic leukemia, Granulocytosis

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Control of cell cycle progression by c-Jun is p-53 dependent

Article Abstract:

Fibroblasts that are taken from c-jun -/- mouse fetuses have a severe proliferation defect and are in a prolonged crisis before spontaneous immortalization. An essential rate-limiting function of c-Jun in fibroblast proliferation is negative regulation of p53 expression. There is a mechanistic link between c-Jun-dependent cell-cycle regulation and mitogenic signaling.

Observations, Cellular signal transduction, Cell cycle, Mice, mutant strains, Mutant mice, Cell proliferation

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