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p38b  -  p38b MAP kinase

Drosophila melanogaster

Synonyms: 186F5S, BG:DS00797.3, CG7393, D-p38, D-p38 MAPK, ...
 
 
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High impact information on p38b

  • The Drosophila p38 MAPK pathway is required during oogenesis for egg asymmetric development [1].
  • Furthermore, they show that in addition to the well-characterized Ras/Raf/ERK MAPK pathway acting in the follicle cells, another related signaling cascade, the p38 MAPK pathway, is required in the germ line for correct axes determination [1].
  • Expression of a dominant-negative D-p38b in the wing imaginal disc caused a decapentaplegic (dpp)-like phenotype and enhanced the phenotype of a dpp mutant [2].
  • The fruit fly, Drosophila melanogaster, has two p38 genes, D-p38a and D-p38b [2].
  • Inhibition of D-p38b function also caused the suppression of the wing phenotype induced by constitutively active Tkv (TkvCA) [2].
 

Biological context of p38b

  • The results revealed that one of the functions of D-p38 is to attenuate antimicrobial peptide gene expression following exposure to lipopolysaccharide [3].
  • p38 mitogen-activated protein kinase can be involved in transforming growth factor beta superfamily signal transduction in Drosophila wing morphogenesis [2].
  • In our previous report, it was proposed that P. aeruginosa secreting ExoS, upon infection, shuts down host cell survival signal pathways by inhibiting ERK1/2 and p38 activation, and it activates proapoptotic pathways through activation of JNK1/2, leading ultimately to cytochrome c release and activation of caspases [4].
  • However, unlike mammalian p38 MAPK, the addition of lipopolysaccharide (LPS) did not significantly affect the phosphorylation of Dp38 in the LPS-responsive l(2)mbn cell line [5].
 

Anatomical context of p38b

  • Dp38 was rapidly tyrosine 186-phosphorylated in response to osmotic stress, heat shock, serum starvation, and H2O2 in Drosophila l(2)mbn and Schneider cell lines [5].
 

Associations of p38b with chemical compounds

  • Pre-treatment of Schneider cells with inhibitors of PKC, PP 1/2A, p38 MAPK, JNK and proteasomes resulted in the inhibition of morphological differentiation induced by NCS [6].
  • HU-induced differentiation was inhibited upon pretreatment of cells with chemical inhibitors of PP 1/2A, p38 MAPK, JNK, and proteasome [7].
  • Following osmotic stress, tyrosine 186-phosphorylated forms of Dp38 MAPK were detected exclusively in nuclear regions of Schneider cells [5].
 

Other interactions of p38b

  • Ectopic expression of dMLK either in Drosophila S2 or in mammalian HEK293 cells leads to activation of JNK, p38 and extracellular signal regulated kinase (ERK) pathways [8].
  • Activating transcription factor (ATF)-2 is a member of the ATF/cAMP response element-binding protein family of transcription factors, and its trans-activating capacity is enhanced by stress-activated protein kinases such as c-Jun NH(2)-terminal kinase (JNK) and p38 [9].
  • Drosophila activating transcription factor-2 is involved in stress response via activation by p38, but not c-Jun NH(2)-terminal kinase [9].
 

Analytical, diagnostic and therapeutic context of p38b

  • These results demonstrate that p38, in addition to its role as a transducer of emergency stress signaling, may function to modulate Dpp signaling [2].
  • The cDNA sequence analysis showed that this Drosophila kinase is a homologue of mammalian p38 MAPK and the yeast HOG1 gene and thus was referred to as Dp38 [5].

References

  1. The Drosophila p38 MAPK pathway is required during oogenesis for egg asymmetric development. Suzanne, M., Irie, K., Glise, B., Agnès, F., Mori, E., Matsumoto, K., Noselli, S. Genes Dev. (1999) [Pubmed]
  2. p38 mitogen-activated protein kinase can be involved in transforming growth factor beta superfamily signal transduction in Drosophila wing morphogenesis. Adachi-Yamada, T., Nakamura, M., Irie, K., Tomoyasu, Y., Sano, Y., Mori, E., Goto, S., Ueno, N., Nishida, Y., Matsumoto, K. Mol. Cell. Biol. (1999) [Pubmed]
  3. A conserved p38 mitogen-activated protein kinase pathway regulates Drosophila immunity gene expression. Han, Z.S., Enslen, H., Hu, X., Meng, X., Wu, I.H., Barrett, T., Davis, R.J., Ip, Y.T. Mol. Cell. Biol. (1998) [Pubmed]
  4. Expression of Pseudomonas aeruginosa Toxin ExoS Effectively Induces Apoptosis in Host Cells. Jia, J., Wang, Y., Zhou, L., Jin, S. Infect. Immun. (2006) [Pubmed]
  5. Molecular cloning and characterization of a Drosophila p38 mitogen-activated protein kinase. Han, S.J., Choi, K.Y., Brey, P.T., Lee, W.J. J. Biol. Chem. (1998) [Pubmed]
  6. Myogenic differentiation of Drosophila Schneider cells by DNA double-strand break-inducing drugs. Hossain, M.S., Akimitsu, N., Kurokawa, K., Sekimizu, K. Differentiation (2003) [Pubmed]
  7. Induction of fusion-competent myoblast-specific gene expression during myogenic differentiation of Drosophila Schneider cells by DNA double-strand breaks or replication inhibition. Hossain, M.S., Kurokawa, K., Sekimizu, K. Biochim. Biophys. Acta (2005) [Pubmed]
  8. Drosophila mixed lineage kinase/slipper, a missing biochemical link in Drosophila JNK signaling. Sathyanarayana, P., Barthwal, M.K., Lane, M.E., Acevedo, S.F., Skoulakis, E.M., Bergmann, A., Rana, A. Biochim. Biophys. Acta (2003) [Pubmed]
  9. Drosophila activating transcription factor-2 is involved in stress response via activation by p38, but not c-Jun NH(2)-terminal kinase. Sano, Y., Akimaru, H., Okamura, T., Nagao, T., Okada, M., Ishii, S. Mol. Biol. Cell (2005) [Pubmed]
 
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