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Docking protein 1, 62kDa

Dok-1, Dok, p62dok, p62(dok), downstream of tyrosine kinase
The protein encoded by this gene is part of a signal transduction pathway downstream of receptor tyrosine kinases. The encoded protein is a scaffold protein that helps form a platform for the assembly of multiprotein signaling complexes. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2010] (from NCBI)
Top mentioned proteins: Src, CAN, GAP, Dok-2, V1a
Papers on Dok-1
Dominant de novo DSP mutations cause erythrokeratodermia-cardiomyopathy syndrome.
Choate et al., Chicago, United States. In Hum Mol Genet, Feb 2016
Disorders of keratinization (DOK) show marked genotypic and phenotypic heterogeneity.
Effective Treatment With Albuterol in DOK7 Congenital Myasthenic Syndrome in Children.
Tsao, Columbus, United States. In Pediatr Neurol, Jan 2016
DOK7 (downstream of tyrosine kinase 7) congenital myasthenic syndrome was previously treated successfully with ephedrine and salbutamol; however, both are unavailable in the United States.
Interleukin-1 beta transactivates epidermal growth factor receptor via the CXCL1-CXCR2 axis in oral cancer.
Shieh et al., Taiwan. In Oncotarget, Dec 2015
Previously, we reported that OSCC cells secrete interleukin-1 beta (IL-1β), which promotes the proliferation of the oral premalignant cell line, DOK, and stimulates DOK and OSCC cells to produce the chemokine CXCL1.
High expression of survivin and its splice variants survivin ΔEx3 and survivin 2 B in oral cancers.
Teni et al., Mumbai, India. In Oral Surg Oral Med Oral Pathol Oral Radiol, Oct 2015
MATERIALS AND METHODS: The expression of 6 survivin isoforms in 4 oral cancer cell lines (AW8507, AW13516, UPCI-SCC040, UPCI-SCC029 B), a dysplastic oral cell line (DOK), 75 paired oral tumor and adjacent normal tissues, and 12 normal oral tissue samples from healthy individuals was analyzed by real-time PCR.
Peroxiredoxin 1 suppresses apoptosis via regulation of the apoptosis signal-regulating kinase 1 signaling pathway in human oral leukoplakia.
Tang et al., Beijing, China. In Oncol Lett, Sep 2015
The interaction between Prx1 and ASK1 was examined in H2O2-treated DOK cells by glutathione-S-transferase pull-down assays and by co-immunoprecipitation in vitro.
IL-37 requires the receptors IL-18Rα and IL-1R8 (SIGIRR) to carry out its multifaceted anti-inflammatory program upon innate signal transduction.
Nold et al., Melbourne, Australia. In Nat Immunol, Apr 2015
Proteomic and transcriptomic investigations revealed that IL-37 used IL-1R8 to harness the anti-inflammatory properties of the signaling molecules Mer, PTEN, STAT3 and p62(dok) and to inhibit the kinases Fyn and TAK1 and the transcription factor NF-κB, as well as mitogen-activated protein kinases.
Development and application of PI3K assays for novel drug discovery.
Giri et al., Hyderābād, India. In Expert Opin Drug Discov, Feb 2015
INTRODUCTION: Phosphoinositide 3-kinases (PI3Ks) constitute one of the most important signaling pathways, playing a vital role in cellular differentiation and proliferation with a key function in cellular receptor triggered signal transduction downstream of tyrosine kinase receptors and/or G-protein coupled receptors.
Sorbs1 and -2 Interact with CrkL and Are Required for Acetylcholine Receptor Cluster Formation.
Glass et al., Cambridge, United States. In Mol Cell Biol, 2014
Crk and CrkL are noncatalytic adaptor proteins necessary for the formation of neuromuscular synapses which function downstream of muscle-specific kinase (MuSK), a receptor tyrosine kinase expressed in skeletal muscle, and the MuSK binding protein Dok-7.
Neuromuscular disease. DOK7 gene therapy benefits mouse models of diseases characterized by defects in the neuromuscular junction.
Yamanashi et al., Tokyo, Japan. In Science, 2014
The muscle protein Dok-7 is essential for activation of the receptor kinase MuSK, which governs NMJ formation, and DOK7 mutations underlie familial limb-girdle myasthenia (DOK7 myasthenia), a neuromuscular disease characterized by small NMJs.
Pharmacologic treatment of downstream of tyrosine kinase 7 congenital myasthenic syndrome.
Vissing et al., Copenhagen, Denmark. In Jama Neurol, 2014
OBJECTIVE: To analyze the information published thus far concerning the effect of pharmacologic treatment of one of the most common subtypes of CMS, downstream of tyrosine kinase 7 (DOK7) CMS.
The role of MuSK in synapse formation and neuromuscular disease.
Zhang et al., New York City, United States. In Cold Spring Harb Perspect Biol, 2013
In addition, MuSK phosphorylation is stimulated by an inside-out ligand, docking protein-7 (Dok-7), which is recruited to tyrosine-phosphorylated MuSK and increases MuSK kinase activity.
Beyond 'furballs' and 'dumpling soups' - towards a molecular architecture of signaling complexes and networks.
Feller et al., Oxford, United Kingdom. In Febs Lett, 2012
Similarly, many growth factor receptors, for example EGF receptor, insulin receptor and c-Met, signal via huge protein complexes built on large platform proteins (Gab, Irs/Dok, p130Cas[BCAR1], Frs families etc.), which are structurally not well understood.
Inactivation of the putative suppressor gene DOK1 by promoter hypermethylation in primary human cancers.
Sylla et al., Lyon, France. In Int J Cancer, 2012
hypermethylation of DOK1 is a potentially critical event in human carcinogenesis.
The inositol 5-phosphatase SHIP-1 and adaptors Dok-1 and 2 play central roles in CD4-mediated inhibitory signaling.
Cambier et al., Denver, United States. In Immunol Lett, 2012
Studies using SHIP-1 shRNA, knockout mice and decoy inhibitors further indicate that CD4-mediated inhibition of TCR-mediated T cell activation is SHIP-1 and Dok-1/2 dependent, and involves SHIP-1 hydrolysis of Phosphatidylinositol 3,4,5-trisphosophate
Dok-1 and Dok-2 deficiency induces osteopenia via activation of osteoclasts.
Noda et al., Tokyo, Japan. In J Cell Physiol, 2011
Dok-1 and Dok-2 deficiency induces osteopenia by activation of osteoclasts.
An essential regulatory role of downstream of kinase-1 in the ovalbumin-induced murine model of asthma.
Park et al., Pusan, South Korea. In Plos One, 2011
Studies demonstrate DOK-1 regulates allergen-induced Th2 immune responses by selective stimulation and inhibition of STAT-4 and STAT-6 signaling pathways, respectively.
Monophosphorylation of CD79a and CD79b ITAM motifs initiates a SHIP-1 phosphatase-mediated inhibitory signaling cascade required for B cell anergy.
Cambier et al., Denver, United States. In Immunity, 2011
In studies reported here, Src homology-2 (SH2)-containing inositol 5-phosphatase SHIP-1 and its adaptor Dok-1 were found to be constitutively phosphorylated in anergic B cells, and activation of this inhibitory circuit was dependent on Src-family kinase activity and consequent to biased BCR immunoreceptor tyrosine-based activation motif (ITAM) monophosphorylation.
Characterization of DOK1, a candidate tumor suppressor gene, in epithelial ovarian cancer.
Bachvarov et al., Québec, Canada. In Mol Oncol, 2011
These findings are suggestive for a possible tumor suppressor role of DOK1 in epithelial ovarian cancer.
B cell receptor-mediated antigen gathering requires ubiquitin ligase Cbl and adaptors Grb2 and Dok-3 to recruit dynein to the signaling microcluster.
Batista et al., London, United Kingdom. In Immunity, 2011
Here, through a combination of high-resolution imaging, genetics and quantitative mass spectrometry, we demonstrate that adaptors Grb2 and Dok-3, and ubiquitin ligase Cbl in signaling BCR microclusters mediate association with the microtubule motor dynein.
Identification of DOK genes as lung tumor suppressors.
Pandolfi et al., Boston, United States. In Nat Genet, 2010
Identification of DOK genes as lung tumor suppressors.
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