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The protein encoded by DOK1 is part of a signal transduction pathway downstream of receptor tyrosine kinases. Zusätzlich bieten wir Ihnen DOK1 Kits (11) und DOK1 Proteine (9) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal DOK1 Primary Antibody für IHC - ABIN966767
Wick, Dong, Hu, Langlais, Liu: Insulin receptor-mediated p62dok tyrosine phosphorylation at residues 362 and 398 plays distinct roles for binding GTPase-activating protein and Nck and is essential for inhibiting insulin-stimulated activation of Ras and Akt. in The Journal of biological chemistry 2001
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Human Polyclonal DOK1 Primary Antibody für IHC - ABIN966766
Songyang, Yamanashi, Liu, Baltimore: Domain-dependent function of the rasGAP-binding protein p62Dok in cell signaling. in The Journal of biological chemistry 2001
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Human DOK1 Primary Antibody für IHC - ABIN966764
Némorin, Duplay: Evidence that Llck-mediated phosphorylation of p56dok and p62dok may play a role in CD2 signaling. in The Journal of biological chemistry 2000
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Human DOK1 Primary Antibody für IHC - ABIN966765
Simoncic, Bourdeau, Lee-Loy, Rohrschneider, Tremblay, Stanley, McGlade: T-cell protein tyrosine phosphatase (Tcptp) is a negative regulator of colony-stimulating factor 1 signaling and macrophage differentiation. in Molecular and cellular biology 2006
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Human Polyclonal DOK1 Primary Antibody für WB - ABIN515056
Barrett, Evans, Frolov, Britton, Pellet-Many, Yamaji, Mehta, Bandopadhyay, Li, Brandner, Zachary, Frankel: A crucial role for DOK1 in PDGF-BB-stimulated glioma cell invasion through p130Cas and Rap1 signalling. in Journal of cell science 2014
Taken together, these results indicate that ATRA-enhanced expression of DOK1 activates PPARgamma (zeige PPARG Antikörper) leading to inhibition of cell proliferation and enhancement of cell apoptosis in MCF-7 cell.
DOK1 was identified as a prognostic factor for non-metastatic CRC (zeige CALR Antikörper), and, via its drugability by PPARgamma (zeige PPARG Antikörper)-agonist, may constitute a potential target for future cancer treatments.
DOK3 (zeige DOK3 Antikörper) expression was not altered much in HTLV-1-infected T cells.
Results indicate that hypermethylation of tumor suppressor protein (zeige TP53 Antikörper) RASSF1A (zeige RASSF1 Antikörper) and docking protein 1 (DOK1) contributes to hepatocarcinogenesis and is associated to clinicopathological characteristics.
Data show that residues Ser745 and Ser756 in the integrin beta2 tail, which are adjacent to the NxxF motif, are required for docking protein 1, docking protein 1, 62kDa (zeige GTF2H1 Antikörper) (downstream of tyrosine kinase 1) (Dok1) interaction.
results support a model in which Dok1 phosphorylation normally suppresses localized Ras pathway activity in Crk (zeige CRK Antikörper)-transformed cells via recruitment and/or activation of RasGAP (zeige RASA1 Antikörper)
Data implicate existence of alternate conformational states around the ligand binding pocket of the PTB (zeige PTBP1 Antikörper) domain of phosphoprotien Dok1 either in the native or in the near native conditions.
Deregulation of DOK1 gene expression by EBV and novel insights into the regulation of the DOK1 tumor suppressor in viral-related carcinogenesis.
point mutations in DOK1 and DOK2 genes are detected with low frequency in chronic myelomonocytic leukemia but may have consequences for the function of the DOK2 PTB (zeige PTBP1 Antikörper) domain
A crucial role for DOK1 in the regulation of PDGF-BB-mediated tumour cell motility through a p130Cas-Rap1 signalling pathway.
findings demonstrate that Dok-3 (zeige DOK3 Antikörper) and Dok-1/-2 play distinctive but cooperative roles in osteoclastogenesis and protect mice from osteopenia, providing physiological and pathophysiological insight into bone homeostasis.
Platelets from Dok-1-/- mice displayed normal aggregation, activation of integrin alphaIIbbeta3, P-selectin (zeige SELP Antikörper) surface expression, and soluble fibrinogen binding. These findings indicate that Dok-1 does not affect "inside-out" platelet signalling.
in the absence of PAG, Csk becomes more associated with alternative partners; i.e., phosphatase PTPN22 and Dok adaptors. Combining PAG deficiency with PTPN22 or Dok adaptor deficiency further enhances effector T cell responses. Unlike PAG, Cbl ubiquitin ligases inhibit the activation of naive, but not of effector, T cells.
These results reveal the critical involvement of Dok-1 and Dok-2 in a negative-feedback loop that prevents overactivation of CD8 (zeige CD8A Antikörper)(+) T cells and promotes memory formation.
Thus, Dok-1 and Dok-2 promote survival of glycoprotein B-specific CD8 (zeige CD8A Antikörper)(+) T cells in trigeminal ganglia latently infected with herpes simplex virus 1.
this study shows that Dok1 and Dok2 proteins are involved in the control of hematopoietic stem cell cycle regulation
Taken together, our results demonstrate that Dok-1 and Dok-2 negatively regulate intestinal inflammation, apparently through the induction of IL-17A (zeige IL17A Antikörper) and IL-22 (zeige IL22 Antikörper) expression.
Dok1 knockdown attenuated TLR2-induced NF-kappaB (zeige NFKB1 Antikörper) activation and IL-6 (zeige IL6 Antikörper) production in microglia.
Triple Dok1 Doc2 (zeige DOC2A Antikörper) Doc3 knockout leads to spontaneous pulmonary inflammation with hallmarks of asthma.
Dok-1 overexpression promotes the generation of an innate-like CD8 (zeige CD8A Antikörper)(+) T-cell population that expresses Eomesodermin (zeige EOMES Antikörper).
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.
Downstream of tyrosine kinase 1
, docking protein 1
, docking protein 1 (downstream of tyrosine kinase 1)
, downstream of tyrosine kinase 1
, downstream of tyrosine kinase-1