Cell cycle reentry of mammalian fibroblasts is accompanied by the sustained activation of p44mapk and p42mapk isoforms in the G1 phase and their inactivation at the G1/S transition - PubMed (original) (raw)
Cell cycle reentry of mammalian fibroblasts is accompanied by the sustained activation of p44mapk and p42mapk isoforms in the G1 phase and their inactivation at the G1/S transition
S Meloche. J Cell Physiol. 1995 Jun.
Abstract
Mitogen-activated protein (MAP) kinases are serine/threonine kinases that are rapidly activated in response to mitogenic stimuli. Here we examined the enzymatic activity and phosphorylation state of the individual p44mapk and p42mapk isoforms during early G1 and late G1 phase of the mammalian cell cycle. Release of fibroblast cells from early G1 block was accompanied by a rapid rise in the myelin basic protein (MBP) kinase activity of p44mapk and p42mapk, which declined slowly over several hours to reach negligible values as cells enter S phase. When cells were released from late G1 block, the activity of p44mapk and p42mapk increased transiently, and then rapidly declined to baseline values during G1 to S phase transition. Cells released at the G1/S boundary in a medium lacking growth factors entered S phase in the complete absence of MAP kinase activity. Unlike MAP kinases, the histone H1 kinase activity of p33cdk2 was elevated in late G1 arrested cells and continued to increase during S phase entry. The enzymatic activation of p44mapk and p42mapk in both early G1 and late G1 phase was accompanied by an increase in the phosphothreonine and phosphotyrosine content of the proteins. These findings suggest that the sustained activation of MAP kinases during G1 progression and their inactivation at the G1/S transition are two regulatory processes involved in the mitogenic response to growth factors.
Similar articles
- Growth factors induce nuclear translocation of MAP kinases (p42mapk and p44mapk) but not of their activator MAP kinase kinase (p45mapkk) in fibroblasts.
Lenormand P, Sardet C, Pagès G, L'Allemain G, Brunet A, Pouysségur J. Lenormand P, et al. J Cell Biol. 1993 Sep;122(5):1079-88. doi: 10.1083/jcb.122.5.1079. J Cell Biol. 1993. PMID: 8394845 Free PMC article. - Fluoride at mitogenic doses induces a sustained activation of p44mapk, but not p42mapk, in human TE85 osteosarcoma cells.
Wu LW, Yoon HK, Baylink DJ, Graves LM, Lau KH. Wu LW, et al. J Clin Endocrinol Metab. 1997 Apr;82(4):1126-35. doi: 10.1210/jcem.82.4.3886. J Clin Endocrinol Metab. 1997. PMID: 9100584 - Structural analysis of the MAP kinase ERK2 and studies of MAP kinase regulatory pathways.
Cobb MH, Xu S, Cheng M, Ebert D, Robbins D, Goldsmith E, Robinson M. Cobb MH, et al. Adv Pharmacol. 1996;36:49-65. doi: 10.1016/s1054-3589(08)60576-1. Adv Pharmacol. 1996. PMID: 8783554 Review. No abstract available.
Cited by
- NAK-associated protein 1/NAP1 activates TBK1 to ensure accurate mitosis and cytokinesis.
Paul S, Sarraf SA, Nam KH, Zavar L, DeFoor N, Biswas SR, Fritsch LE, Yaron TM, Johnson JL, Huntsman EM, Cantley LC, Ordureau A, Pickrell AM. Paul S, et al. J Cell Biol. 2024 Feb 5;223(2):e202303082. doi: 10.1083/jcb.202303082. Epub 2023 Dec 7. J Cell Biol. 2024. PMID: 38059900 Free PMC article. - Computational evidence for multi-layer crosstalk between the cadherin-11 and PDGFR pathways.
Karagöz Z, Passanha FR, Robeerst L, van Griensven M, LaPointe VLS, Carlier A. Karagöz Z, et al. Sci Rep. 2023 Sep 22;13(1):15804. doi: 10.1038/s41598-023-42624-x. Sci Rep. 2023. PMID: 37737289 Free PMC article. - Neurodevelopmental disorders, like cancer, are connected to impaired chromatin remodelers, PI3K/mTOR, and PAK1-regulated MAPK.
Nussinov R, Yavuz BR, Arici MK, Demirel HC, Zhang M, Liu Y, Tsai CJ, Jang H, Tuncbag N. Nussinov R, et al. Biophys Rev. 2023 Apr 1;15(2):163-181. doi: 10.1007/s12551-023-01054-9. eCollection 2023 Apr. Biophys Rev. 2023. PMID: 37124926 Free PMC article. Review. - ERK1/ATF-2 signaling axis contributes to interleukin-1β-induced MMP-3 expression in dermal fibroblasts.
Kitanaka N, Nakano R, Sakai M, Kitanaka T, Namba S, Konno T, Nakayama T, Sugiya H. Kitanaka N, et al. PLoS One. 2019 Sep 19;14(9):e0222869. doi: 10.1371/journal.pone.0222869. eCollection 2019. PLoS One. 2019. PMID: 31536594 Free PMC article. - High Glucose Environments Interfere with Bone Marrow-Derived Macrophage Inflammatory Mediator Release, the TLR4 Pathway and Glucose Metabolism.
Ayala TS, Tessaro FHG, Jannuzzi GP, Bella LM, Ferreira KS, Martins JO. Ayala TS, et al. Sci Rep. 2019 Aug 7;9(1):11447. doi: 10.1038/s41598-019-47836-8. Sci Rep. 2019. PMID: 31391499 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous