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.

User Contributions:

Comment about this article or add new information about this topic:

Comment:  (50-4000 characters)

Name:

E-mail:

Security Code:

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.

User Contributions:

Comment about this article or add new information about this topic:

Comment:  (50-4000 characters)

Name:

E-mail:

Security Code:

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.

User Contributions:

Comment about this article or add new information about this topic:

Comment:  (50-4000 characters)

Name:

E-mail:

Security Code: