ArticleThe Journal of biological chemistry2010
p38 MAP kinase and MAPKAP kinases MK2/3 cooperatively phosphorylate epithelial keratins.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- CK8/18 and Claudin Profile of Female Breast Cancers from Botswana.Breast cancer : basic and clinical research · 2026Article
- Liquiritin Suppresses Intracellular and Secreted MUC5AC and MUC5B in Human Airway Epithelial Cells.International journal of molecular sciences · 2025Article
- SRC and ERK Regulate the Turnover of Cytoskeletal Keratin Filaments.International journal of molecular sciences · 2025Article
- Musashi-2 Deficiency Triggers Colorectal Cancer Ferroptosis by Downregulating the MAPK Signaling Cascade to Inhibit HSPB1 Phosphorylation.Biological procedures online · 2023Article
- Mitogen-activated protein kinase-activated protein kinase-2 (MK2) and its role in cell survival, inflammatory signaling, and migration in promoting cancer.Molecular carcinogenesis · 2022Article
- Article
- An ultrasensitive fiveplex activity assay for cellular kinases.Scientific reports · 2019Article
- A novel function for the MAP kinase SMA-5 in intestinal tube stability.Molecular biology of the cell · 2016Article
- GTPase domain driven dimerization of SEPT7 is dispensable for the critical role of septins in fibroblast cytokinesis.Scientific reports · 2016Article
- Phosphorylation and Reorganization of Keratin Networks: Implications for Carcinogenesis and Epithelial Mesenchymal Transition.Biomolecules & therapeutics · 2015Review
- p38MAPK/MK2-mediated phosphorylation of RBM7 regulates the human nuclear exosome targeting complex.RNA (New York, N.Y.) · 2015Article
- MAPK-Activated Protein Kinases (MKs): Novel Insights and Challenges.Frontiers in cell and developmental biology · 2015Review
- Genetic deletion of SEPT7 reveals a cell type-specific role of septins in microtubule destabilization for the completion of cytokinesis.PLoS genetics · 2014Article
- MAPKAP kinase 2 (MK2)-dependent and -independent models of blister formation in pemphigus vulgaris.The Journal of investigative dermatology · 2014Article
- Peptide-mediated desmoglein 3 crosslinking prevents pemphigus vulgaris autoantibody-induced skin blistering.The Journal of clinical investigation · 2013Article
- "Panta rhei": Perpetual cycling of the keratin cytoskeleton.Bioarchitecture · 2011Article
- SB202190-induced cell type-specific vacuole formation and defective autophagy do not depend on p38 MAP kinase inhibition.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The MAPK-activated protein kinases (MAPKAP kinases) MK2 and MK3 are directly activated via p38 MAPK phosphorylation, stabilize p38 by complex formation, and contribute to the stress response. The list of substrates of MK2/3 is increasing steadily. We applied a phosphoproteomics approach to compare protein phosphorylation in MK2/3-deficient cells rescued or not by ectopic expression of MK2. In addition to differences in phosphorylation of the known substrates of MK2, HSPB1 and Bag-2, we identified strong differences in phosphorylation of keratin 8 (K8). The phosphorylation of K8-Ser(73) is catalyzed directly by p38, which in turn shows MK2-dependent expression. Notably, analysis of small molecule p38 inhibitors on K8-Ser(73) phosphorylation also demonstrated reduced phosphorylations of keratins K18-Ser(52) and K20-Ser(13) but not of K8-Ser(431) or K18-Ser(33). Interestingly, K18-Ser(52) and K20-Ser(13) are not directly phosphorylated by p38 in vitro, but by MK2. Furthermore, anisomycin-stimulated phosphorylations of K20-Ser(13) and K18-Ser(52) are inhibited by small molecule inhibitors of both p38 and MK2. MK2 knockdown in HT29 cells leads to reduced K20-Ser(13) phosphorylation, which further supports the notion that MK2 is responsible for K20 phosphorylation in vivo. Physiologic relevance of these findings was confirmed by differences of K20-Ser(13) phosphorylation between the ileum of wild-type and MK2/3-deficient mice and by demonstrating p38- and MK2-dependent mucin secretion of HT29 cells. Therefore, MK2 and p38 MAPK function in concert to phosphorylate K8, K18, and K20 in intestinal epithelia.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.