Receptor protein tyrosine kinase DDR is up‐regulated by p53 protein
@article{Sakuma1996ReceptorPT, title={Receptor protein tyrosine kinase DDR is up‐regulated by p53 protein}, author={Shirou Sakuma and Hideyuki Saya and Mitsuhiro Tada and M Nakao and Toshiyoshi Fujiwara and Jack A. Roth and Yutaka Sawamura and Yumiko Shinohe and Hiroshi Abe}, journal={FEBS Letters}, year={1996}, volume={398} }
41 Citations
p53 induction and activation of DDR1 kinase counteract p53‐mediated apoptosis and influence p53 regulation through a positive feedback loop
- BiologyThe EMBO journal
- 2003
DDR1, discoidin domain receptor 1, belongs to a subfamily of tyrosine kinase receptors with an extracellular domain homologous to Dictyostellium discoideum protein discoidin 1. We showed that DDR1 is…
Transcriptional control of human p53-regulated genes
- BiologyNature Reviews Molecular Cell Biology
- 2008
The most comprehensive list so far of human p53-regulated genes and their experimentally validated, functional binding sites that confer p53 regulation is presented.
Differential Recognition of Response Elements Determines Target Gene Specificity forp53 and p63
- BiologyMolecular and Cellular Biology
- 2005
The results indicate that p63 can regulate expression of specific target genes such as those involved in skin, limb, and craniofacial development by preferentially activating distinct p63-specific response elements.
Identification of Receptor Tyrosine Kinase, Discoidin Domain Receptor 1 (DDR1), as a Potential Biomarker for Serous Ovarian Cancer
- BiologyInternational journal of molecular sciences
- 2011
The results suggest that the expression of DDR1 may serve as both a potential biomarker and a molecular target for advanced ovarian cancer.
Identification of two novel, kinase‐deficient variants of discoidin domain receptor 1: differential expression in human colon cancer cell lines
- BiologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
- 2001
Exogenous overexpression of DDR1d in transient transfection assays supported a nondominant negative mechanism of signal modulation, and stimulation with collagen induced full‐length receptor phosphorylation suggested a lack of dominant‐negative inhibition by DDR1D.
Human Cancer Biology InhibitionofCollagenReceptorDiscoidinDomainReceptor-1 ( DDR 1 ) Reduces Cell Survival , Homing , and Colonization in Lung Cancer Bone Metastasis
- Biology, Medicine
- 2012
The role of the collagen-binding receptor discoidin domain receptor-1 (DDR1) in the initiation and development of bone metastasis is investigated in lung cancer specimens and phosphorylation status in a panel of human lung cancer cell lines is examined.
Discoidin domain receptor tyrosine kinases: new players in cancer progression
- BiologyCancer and Metastasis Reviews
- 2012
This review summarizes and discusses the current knowledge on DDR expression and function in cancer, and hopes that this effort will encourage more research into these poorly understood but unique RTKs, which have the potential of becoming novel therapeutic targets in cancer.
An investigation of the aberrant expression and activation of receptor tyrosine kinases in hodgkin’s lymphoma
- Biology
- 2011
It is shown that HL cells are sensitive to the RTK inhibitor, dasatinib, and consistent with the aberrant activation of multiple RTKs in HL cells, these cells were also sensitive to lestaurtinib and dovitinib, two next generation multiple-target RTK inhibitors.
Discoidin domain receptor 1 isoform‐a (DDRla) promotes migration of leukocytes in three‐dimensional collagen lattices
- Biology, MedicineFASEB journal : official publication of the Federation of American Societies for Experimental Biology
- 2001
It is proposed that the interaction of DDR1a with collagen of the ECM results in a requisite intracellular signaling that enables leukocytes to migrate in a tissue microenvironment and participate in host defense.
Contribution of p53 to metastasis.
- Biology, MedicineCancer discovery
- 2014
Understanding the mechanisms by which p53 loss and mutation promote tumor metastasis is crucial to understanding the biology of tumor progression and how to appropriately apply targeted therapies.
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