Transcription factor ATF2 regulation by the JNK signal transduction pathway.

Transcription factor ATF2 regulation by the JNK signal transduction pathway.

Science (New York, N.Y.) (1995-01-20)

S Gupta, D Campbell, B Dérijard, R J Davis

RESUMEN

Treatment of cells with pro-inflammatory cytokines or ultraviolet radiation causes activation of the c-Jun NH2-terminal protein kinase (JNK). Activating transcription factor-2 (ATF2) was found to be a target of the JNK signal transduction pathway. ATF2 was phosphorylated by JNK on two closely spaced threonine residues within the NH2-terminal activation domain. The replacement of these phosphorylation sites with alanine inhibited the transcriptional activity of ATF2. These mutations also inhibited ATF2-stimulated gene expression mediated by the retinoblastoma (Rb) tumor suppressor and the adenovirus early region 1A (E1A) oncoprotein. Furthermore, expression of dominant-negative JNK inhibited ATF2 transcriptional activity. Together, these data demonstrate a role for the JNK signal transduction pathway in transcriptional responses mediated by ATF2.

MATERIALES

Referencia del producto

Marca

Descripción del producto

14-328

Sigma-Aldrich

JNK1α1/SAPK1c Protein, inactive, 50 g, Unactive, N-terminal His6-tagged recombinant, human, full-length JNK1α1/SAPK1c, for use in Kinase Assays.

14-329-M

Sigma-Aldrich

JNK2α2/SAPK1a Protein, active, 10 µg, Active, N-terminal His-tagged, full length human JNK2α2/SAPK1a, for use in Kinase Assays.

14-327-M

Sigma-Aldrich

JNK1α1/SAPK1c Protein, active, 10 µg, Active, recombinant full-length human JNK1α1/SAPK1c with an N-terminal His-tag, for use in Kinase Assays.

14-330

Sigma-Aldrich

JNK2α2/SAPK1a Protein, inactive, 50 g, Unactive, N-terminal His6-tagged, recombinant, full-length, human JNK2α2/SAPK1a unactive, for use in Kinase Assays.