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PTPRJ promotes osteoclast maturation and activity by inhibiting Cbl-mediated ubiquitination of NFATc1 in late osteoclastogenesis.
FEBS J
August 2021
Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Bone-resorbing osteoclasts (OCLs) are multinucleated phagocytes, whose central roles in regulating bone formation and homeostasis are critical for normal health and development. OCLs are produced from precursor monocytes in a multistage process that includes initial differentiation, cell-cell fusion, and subsequent functional and morphological maturation; the molecular regulation of osteoclastogenesis is not fully understood. Here, we identify the receptor-type protein tyrosine phosphatase PTPRJ as an essential regulator specifically of OCL maturation.
View Article and Find Full Text PDFLoss of PTPRJ/DEP-1 enhances NF2/Merlin-dependent meningioma development.
J Neurol Sci
January 2020
Department of Neuropathology, Otto-von-Guericke-University, D-39120 Magdeburg, Germany. Electronic address:
Introduction: Meningiomas are common tumors in adults, which develop from the meningeal coverings of the brain and spinal cord. Loss-of-function mutations or deletion of the NF2 gene, resulting in loss of the encoded Merlin protein, lead to Neurofibromatosis type 2 (NF2), but also cause the formation of sporadic meningiomas. It was shown that inactivation of Nf2 in mice caused meningioma formation.
View Article and Find Full Text PDFLoss of DEP-1 (Ptprj) promotes myeloproliferative disease in -ITD acute myeloid leukemia.
Haematologica
November 2018
Institute of Molecular Cell Biology, Center for Molecular Biomedicine (CMB), Jena University Hospital
β-Integrin de-phosphorylation by the Density-Enhanced Phosphatase DEP-1 attenuates EGFR signaling in C. elegans.
PLoS Genet
January 2017
Institute of Molecular Life Sciences, University of Zürich, Winterthurerstr. 190, University of Zürich, Zürich, Switzerland.
Density-Enhanced Phosphatase-1 (DEP-1) de-phosphorylates various growth factor receptors and adhesion proteins to regulate cell proliferation, adhesion and migration. Moreover, dep-1/scc1 mutations have been detected in various types of human cancers, indicating a broad tumor suppressor activity. During C.
View Article and Find Full Text PDFPositive Regulation of Lyn Kinase by CD148 Is Required for B Cell Receptor Signaling in B1 but Not B2 B Cells.
Immunity
December 2016
Howard Hughes Medical Institute, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center, Departments of Medicine and of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143-0795, USA. Electronic address:
B1 and B2 B cells differ in their ability to respond to T-cell-independent (TI) antigens. Here we report that the Src-family kinase (SFK) regulator CD148 has a unique and critical role in the initiation of B1 but not B2 cell antigen receptor signaling. CD148 loss-of-function mice were found to have defective B1 B-cell-mediated antibody responses against the T-cell-independent antigens NP-ficoll and Pneumovax 23 and had impaired selection of the B1 B cell receptor (BCR) repertoire.
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