| Correlation of distinct behaviors to the modified expression of cerebral Shank1,3 and BDNF in two autistic animal models. | Correlation of distinct behaviors to the modified expression of cerebral Shank1,3 and BDNF in two autistic animal models.
Alò R, Olivito I, Fazzari G, Zizza M, Di Vito A, Avolio E, Mandalà M, Bruno R, Barni T, Canonaco M, Facciolo RM. | 01/22/2022 |
| Dynamic Change of Shanks Gene mRNA Expression and DNA Methylation in Epileptic Rat Model and Human Patients. | Dynamic Change of Shanks Gene mRNA Expression and DNA Methylation in Epileptic Rat Model and Human Patients.
Fu Y, Liu D, Guo J, Long H, Xiao W, Xiao W, Feng L, Luo Z, Xiao B. | 06/5/2021 |
| Loss of scaffold proteins via knockdown of Shank1 or Shank2, but not Shank3, led to a reduction of the number but not the unitary response of AMPAR-containing synapses. Only when both Shank1 and Shank2 were knocked down, were both the number and the unitary response of active synapses reduced. This reduction was accompanied by a decrease in NMDAR-mediated synaptic response. | Shank Proteins Differentially Regulate Synaptic Transmission.
Shi R, Redman P, Ghose D, Hwang H, Liu Y, Ren X, Ding LJ, Liu M, Jones KJ, Xu W., Free PMC Article | 08/11/2018 |
| SHANK1 and SHANK3 act as integrin activation inhibitors by sequestering active Rap1 and R-Ras via the SPN domain and thus limiting their bioavailability at the plasma membrane. | SHANK proteins limit integrin activation by directly interacting with Rap1 and R-Ras.
Lilja J, Zacharchenko T, Georgiadou M, Jacquemet G, De Franceschi N, Peuhu E, Hamidi H, Pouwels J, Martens V, Nia FH, Beifuss M, Boeckers T, Kreienkamp HJ, Barsukov IL, Ivaska J., Free PMC Article | 06/24/2017 |
| Upon depolarization with high K+, neither the intensity nor distribution of label for GKAP changed, but labeling intensity for Shank at the postsynaptic density increased to ~150% of controls. | Differential distribution of Shank and GKAP at the postsynaptic density.
Tao-Cheng JH, Yang Y, Reese TS, Dosemeci A., Free PMC Article | 02/6/2016 |
| All three Shank mRNA isoforms are differentially expressed in the synaptic neuropil. | Alternative polyadenylation and differential expression of Shank mRNAs in the synaptic neuropil.
Epstein I, Tushev G, Will TJ, Vlatkovic I, Cajigas IJ, Schuman EM., Free PMC Article | 08/16/2014 |
| this study provides a new level of understanding of the specificity and structural plasticity of the shank PDZ domain. | The structural flexibility of the shank1 PDZ domain is important for its binding to different ligands.
Lee JH, Park H, Park SJ, Kim HJ, Eom SH. | 06/4/2011 |
| Despite the fact that the betaPIX coiled-coil domain exposes three PDZ binding motifs in the C-termini, the betaPIX trimer associates with a single Shank PDZ. | Structural basis for asymmetric association of the betaPIX coiled coil and shank PDZ.
Im YJ, Kang GB, Lee JH, Park KR, Song HE, Kim E, Song WK, Park D, Eom SH. | 03/29/2010 |
| shank and homer synaptic cluster disassembly is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathways | Disassembly of shank and homer synaptic clusters is driven by soluble beta-amyloid(1-40) through divergent NMDAR-dependent signalling pathways.
Roselli F, Hutzler P, Wegerich Y, Livrea P, Almeida OF., Free PMC Article | 01/21/2010 |
| Results show that dendritic targeting of shank1 mRNA granules involves KIF5C and the KIF5-associated RNA-binding protein staufen1. | Shank1 mRNA: dendritic transport by kinesin and translational control by the 5'untranslated region.
Falley K, Schütt J, Iglauer P, Menke K, Maas C, Kneussel M, Kindler S, Wouters FS, Richter D, Kreienkamp HJ. | 01/21/2010 |
| the rat shank1 PDZ-ligand complex has a class I PDZ interaction and a novel PDZ-PDZ dimerization | Crystal structure of the Shank PDZ-ligand complex reveals a class I PDZ interaction and a novel PDZ-PDZ dimerization.
Im YJ, Lee JH, Park SH, Park SJ, Rho SH, Kang GB, Kim E, Eom SH. | 01/21/2010 |
| PDZ domain of Shank1 and its complex with the C-terminal octapeptide of GKAP were crystallized | Crystallization and preliminary X-ray crystallographic studies of the PDZ domain of Shank1 from Rattus norvegicus.
Park SH, Im YJ, Rho SH, Lee JH, Yang S, Kim E, Eom SH. | 01/21/2010 |
| results suggest that Shank recruits beta PIX and p21-associated kinase to spines for the regulation of postsynaptic structure | The Shank family of postsynaptic density proteins interacts with and promotes synaptic accumulation of the beta PIX guanine nucleotide exchange factor for Rac1 and Cdc42.
Park E, Na M, Choi J, Kim S, Lee JR, Yoon J, Park D, Sheng M, Kim E. | 01/21/2010 |
| The appearance of dendritic Shank mRNAs in cerebellar Purkinje cells coincides with the onset of dendrite formation. Expression of reporter transcripts in hippocampal neurons identifies a 200-nucleotide dendritic targeting element in Shank1 mRNA. | Differential expression and dendritic transcript localization of Shank family members: identification of a dendritic targeting element in the 3' untranslated region of Shank1 mRNA.
Böckers TM, Segger-Junius M, Iglauer P, Bockmann J, Gundelfinger ED, Kreutz MR, Richter D, Kindler S, Kreienkamp HJ. | 01/21/2010 |
| These data revealed a close association between the expression and loss of allodynia and hyperalgesia with changes in the levels of Homer1b/c and Shank1a in the spinal dorsal horn. | Increased levels of Homer1b/c and Shank1a in the post-synaptic density of spinal dorsal horn neurons are associated with neuropathic pain in rats.
Miletic G, Miyabe T, Gebhardt KJ, Miletic V. | 01/21/2010 |
| The proline-rich region present in C termini of CaV1.3a subunit binds to Shank Src homology 3 domain. | Association of CaV1.3 L-type calcium channels with Shank.
Zhang H, Maximov A, Fu Y, Xu F, Tang TS, Tkatch T, Surmeier DJ, Bezprozvanny I., Free PMC Article | 01/21/2010 |
| Promotes the maturation of dendritic spines and the enlargement of spine heads. Postsynaptic expression of Shank also enhances presynaptic function. | Regulation of dendritic spine morphology and synaptic function by Shank and Homer.
Sala C, Piëch V, Wilson NR, Passafaro M, Liu G, Sheng M. | 03/29/2006 |