Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Reddy, S.P. et al.

Reddy, Adiseshaiah, Shapiro, Vuong,

BMK1 ( ERK5) regulates squamous differentiation marker SPRR1B transcription in Clara-like H441 cells.

Various toxicants and carcinogens upregulate the expression of small proline-rich protein 1B (SPRR1B), a squamous differentiation marker, in bronchial epithelial cells both in vivo and in vitro. We have recently shown that phorbol 13-myristate 12-acetate (PMA)-stimulated SPRR1B transcription in Clara-like H441 cells is mainly mediated by activator protein-1 (AP-1) and c-Jun N-terminal kinase-1 (JNK1). Though mitogen-activated protein kinase (MAPK) kinase (MEK)-1/2 pathway inhibitors strongly suppressed both basal and PMA-inducible SPRR1B transcription, overexpression of dominant negative (dn) forms of extracellular signal-regulated kinase (ERK)-1 and/or -2 did not have any significant effect indicating the involvement of another ERK-like MAPK in this pathway. Here, we report for the first time the involvement of ERK5 in PMA-inducible SPRR1B transcription in H441 cells. PMA significantly induced ERK5 activation in H441 cells. Overexpression of dn-ERK5 strongly suppressed both basal and PMA-inducible SPRR1B transcription, whereas wild-type ERK5 upregulated it. Consistent with this, a mutant form of MEK-5, an upstream activator of ERK5, strongly suppressed PMA-inducible promoter activity. However, coexpression of c-Jun restored promoter activation suppressed by dn-ERK5. Thus, in addition to JNK1, the activation of MEK5- ERK5 MAPK pathway probably plays a pivotal role in transcriptional regulation of AP-1- mediated SPRR1B expression in the distal bronchiolar region.[1]

References

BMK1 (ERK5) regulates squamous differentiation marker SPRR1B transcription in Clara-like H441 cells. Reddy, S.P., Adiseshaiah, P., Shapiro, P., Vuong, H. Am. J. Respir. Cell Mol. Biol. (2002) [Pubmed]

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