• Various microbial pathogens target the actin-binding protein cortactin to promote their own uptake, proliferation and spread, and exhibit proposed roles in human cancerogenesis. (mdpi.com)
  • Commercial anti bodies made use of have been, anti cortactin 4F11 monoclonal anti body, anti Src GD11 monoclonal and polyclonal anti phosphoY416 antibodies, and anti actin C4 monoclonal antibody. (bcl-2inhibitors.com)
  • The actin-binding protein cortactin is localized to pre- and postsynaptic structures and translocates in a stimulus-dependent manner between spines and the dendritic compartment, thereby indicating a crucial role for synaptic plasticity and neuronal function. (bvsalud.org)
  • While it is known that cortactin directly binds F-actin, the Arp2/3 complex important for actin nucleation and branching as well as other factors involved in synaptic plasticity processes, its precise role in modulating actin remodeling in neurons needs to be deciphered. (bvsalud.org)
  • These phenotypes might at least in part be explained by alterations in the activity-dependent modulation of synaptic actin in cortactin-deficient neurons. (bvsalud.org)
  • The actin-binding protein, cortactin, in endothelial cells is an important player in regulating the interaction of immune cells with the vascular endothelium. (bvsalud.org)
  • HS1 is an actin regulatory protein and cortactin homolog that is expressed in hematopoietic cells. (nih.gov)
  • 11. A Hip1R-cortactin complex negatively regulates actin assembly associated with endocytosis. (nih.gov)
  • We find SDF1 consolidates actin at the leading process tip by de-repressing calpain protease and increasing proteolysis of branched-actin-supporting cortactin. (jneurosci.org)
  • Moreover, ProSAP1/Shank2 −/− mutants exhibit fewer dendritic spines and show reduced basal synaptic transmission, a reduced frequency of miniature excitatory postsynaptic currents and enhanced N -methyl- d -aspartate receptor-mediated excitatory currents at the physiological level. (nature.com)
  • By comparing the data on ProSAP1/Shank2 −/− mutants with ProSAP2/Shank3αβ −/− mice, we show that different abnormalities in synaptic glutamate receptor expression can cause alterations in social interactions and communication. (nature.com)
  • In this study, we characterized the general neuronal function of cortactin in knockout mice. (bvsalud.org)
  • Additional evidence shows impaired long-term potentiation in cortactin knockout mice together with a complete absence of structural spine plasticity. (bvsalud.org)
  • Here we use cortactin gene-inactivated male and female mice to study the role of this protein in EAE. (bvsalud.org)
  • Inducing EAE by immunization with a myelin oligodendrocyte glycoprotein peptide (MOG35-55) revealed an ameliorated disease course in cortactin gene-deficient female mice compared with WT mice. (bvsalud.org)
  • We here review the recent findings in regard to the roles of SHANK3 in higher brain functions, molecular-biologic studies of the complex expression of Shank3 transcripts and production of SHANK3 isoforms, and behavioral studies of Shank3-mutant mice, including our recent findings, and discuss a novel therapeutic approach for ASD. (nih.gov)
  • 6. Hip1-related mutant mice grow and develop normally but have accelerated spinal abnormalities and dwarfism in the absence of HIP1. (nih.gov)
  • 15. IFNγ contributes to the development of gastric epithelial cell metaplasia in Huntingtin interacting protein 1 related (Hip1r)-deficient mice. (nih.gov)
  • These data provide mechanistic insight into the regulation of interneuron leading process dynamics during neuronal migration in mice and provides insight into how cortactin and DCX , a known human neuronal migration disorder gene, participate in this process. (jneurosci.org)
  • Here we explore the prediction that long-term knockdown of cortactin (CTTN), a component of tubulobulbar complexes (TBCs), disrupts TBCs in Sertoli cells and alters the turnover of basal ectoplasmic specializations (ESs). (bvsalud.org)
  • In PFN1-deficient mammalian cells, Halo-PFN1 or mApple-PFN1 (mAp-PEN1) restored morphological and cytoskeletal functions. (elifesciences.org)
  • This approach combined with specific function-disrupting point-mutants (Y6D and R88E) revealed PFN1 bound to microtubules in live cells. (elifesciences.org)
  • However, proliferation capacity and expression of IL-17A and IFNγ by cortactin-deficient and WT splenocytes did not differ, suggesting that the lack of cortactin does not affect induction of the immune response. (bvsalud.org)
  • The constructs used had been full length wild sort cortactin, plus the following derivatives, the single point mutants W22A and W525K, the double mutant S405,418D, the triple mutant Y421,466,482D, an N ter minal fragment of cortactin containing residues 1 333, as well as a cortactin fragment con taining the SH3 domain aas. (bcl-2inhibitors.com)
  • Expression of HS1 Y378F, Y397F is sufficient to rescue migration of HS1-deficient neutrophils, however, a triple phospho-mutant Y222F, Y378F, Y397F did not rescue migration of HS1-deficient neutrophils. (nih.gov)
  • Mutants are extremely hyperactive and display profound autistic-like behavioural alterations including repetitive grooming as well as abnormalities in vocal and social behaviours. (nature.com)
  • RESULTS Tetraploid populations increase in telomere-deficient vHMECs For the evaluation of ploidy levels in post-stasis vHMEC lines (830 and 440212) throughout the cell tradition, a combination of -tubulin immunofluorescence with fluorescent hybridization (FISH) was performed. (ipa2014.org)
  • We discovered that cortactin phosphorylated at Y-470 recruits the signaling factor Vav2 to activate the small Rho GTPase Rac1, and finally, a cancer cell motility phenotype. (mdpi.com)