Affinage

SHANK1

SH3 and multiple ankyrin repeat domains protein 1 · UniProt Q9Y566

Length
2161 aa
Mass
225.0 kDa
Annotated
2026-06-10
39 papers in source corpus 19 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SHANK1 is a multidomain postsynaptic density scaffold protein that organizes excitatory synapses and is required in vivo for normal dendritic spine morphology, PSD ultrastructure, and basal synaptic strength (PMID:10488079, PMID:18272690). It nucleates the PSD complex through its central PDZ domain, which binds the C-termini of GKAP/SAPAP and other partners including CIRL1 and βPIX; crystallographic work defines a plastic hydrophobic pocket with flexible loops that accommodate diverse C-terminal and internal short linear motifs (PMID:10488079, PMID:10964907, PMID:12136153, PMID:21376703, PMID:38899489). Its proline-rich region links the scaffold to actin-regulatory and small-GTPase signaling by binding the SH3 domain of IRSp53 in a cdc42-regulated manner, while the C-terminus mediates synaptic targeting and Homer1 binding (PMID:12504591, PMID:34113010). SHANK1 expression is controlled at multiple levels: its mRNA is transported into dendrites along microtubules via KIF5C/staufen1 and translated under tight control by a GC-rich 5′ UTR, a non-canonical ACG uORF, and FMRP-bound 3′ UTR G-quadruplexes, with a defined dendritic targeting element directing localization (PMID:15121189, PMID:19416473, PMID:25692235, PMID:24533096), and its transcription is driven by PKA/CREB signaling (PMID:40574425). Functionally, SHANK1 is enriched in parvalbumin-positive interneurons where its loss shifts the hippocampal excitatory/inhibitory balance (PMID:25816842), and ASD-associated missense mutations (R874H, P1812L) converge on downregulation of mGluR1–IP3R1–calcium signaling with spine and LTP deficits, while truncating variants abolish Homer1 binding and synaptic targeting, establishing SHANK1 as a gene linked to autism spectrum disorder (PMID:34113010, PMID:35388181, PMID:37880287). Outside the nervous system, SHANK1 stability and expression are regulated by USP18-mediated deubiquitination and EZH2-mediated H3K27me3 silencing, and it scaffolds MDM2-dependent ubiquitination of Klotho in lung cancer cells (PMID:35468874, PMID:40096187, PMID:41274253).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1999 High

    Establishing that SHANK1 is a PSD scaffold answered where this neuronal protein acts by placing it in the postsynaptic density via direct PDZ-domain binding to GKAP/SAPAP.

    Evidence Yeast two-hybrid, reciprocal Co-IP from rat synaptosomes, co-localization in hippocampal neurons

    PMID:10488079

    Open questions at the time
    • Did not define structural basis of PDZ binding
    • Did not establish in vivo requirement for synapse function
  2. 2000 High

    Identifying CIRL1 as a brain-validated PDZ ligand broadened the scaffold's repertoire of receptor partners at the PSD beyond GKAP.

    Evidence Yeast two-hybrid, in vitro binding, Co-IP from rat brain membranes, subcellular fractionation

    PMID:10964907

    Open questions at the time
    • Functional consequence of CIRL1 anchoring not defined
    • CIRL2 bound in vitro but not in vivo, leaving selectivity unexplained
  3. 2002 Medium

    The PDZ–GKAP co-crystal structure answered how SHANK1 recognizes its scaffold ligands at atomic resolution.

    Evidence X-ray crystallography of peptide-free and GKAP-bound PDZ domain

    PMID:12136153

    Open questions at the time
    • No functional validation in this report
    • Single ligand complex did not address binding plasticity
  4. 2002 Medium

    Mapping the IRSp53 interaction to the proline-rich region connected the scaffold to cdc42/actin-based filopodial signaling, explaining how SHANK1 could couple the PSD to cytoskeletal remodeling.

    Evidence Overlay assay, Co-IP from HEK293 cells, co-expression/localization in transfected cells

    PMID:12504591

    Open questions at the time
    • Shown in heterologous cells, not native synapses
    • Downstream actin effects on spine shape not directly measured
  5. 2004 Medium

    Identifying a 3′ UTR dendritic targeting element answered how SHANK1 mRNA reaches dendrites for local availability.

    Evidence Reporter transcript assays and in situ hybridization in hippocampal/cerebellar neurons

    PMID:15121189

    Open questions at the time
    • Did not identify the trans-acting transport machinery
    • Did not address translational regulation
  6. 2008 High

    The knockout established the in vivo requirement for SHANK1, moving it from a binding partner to a determinant of spine size, PSD composition, and synaptic strength.

    Evidence Shank1−/− mice with EM, electrophysiology, and PSD immunoblotting

    PMID:18272690

    Open questions at the time
    • Cell types responsible for phenotype not resolved
    • Did not separate scaffolding from signaling contributions
  7. 2009 Medium

    Defining KIF5C/staufen1-dependent transport and GC-rich 5′ UTR repression answered how SHANK1 mRNA is moved and held translationally silent in dendrites.

    Evidence Live imaging, dominant-negative interference, brain mRNP co-fractionation, reporter assays

    PMID:19416473

    Open questions at the time
    • Signal that derepresses translation locally not identified
    • IRES-independence left activation mechanism open
  8. 2014 Medium

    Discovery of an ACG uORF and FMRP-bound G-quadruplexes resolved how SHANK1 is translated despite a highly structured 5′ UTR and how FMRP regulates it via 3′ UTR structures.

    Evidence Reporter mutagenesis of the ACG codon; biophysical and in vivo FMRP–G-quadruplex binding assays

    PMID:24533096 PMID:25692235

    Open questions at the time
    • Physiological stimuli engaging the uORF not defined
    • Functional outcome of FMRP regulation on synaptic SHANK1 not quantified
  9. 2011 High

    The PDZ–βPIX structure revealed the plasticity that lets one domain bind diverse ligands, explaining the scaffold's promiscuity.

    Evidence X-ray crystallography at 2.3 Å plus modeling of additional PDZ–peptide complexes

    PMID:21376703

    Open questions at the time
    • Did not test binding hierarchy among competing ligands
    • No mutational test of identified contacts in cells
  10. 2015 High

    Localizing SHANK1 to parvalbumin interneurons answered which circuit element drives the knockout phenotype, linking loss to an excitatory/inhibitory imbalance.

    Evidence Immunofluorescence, mEPSC/mIPSC recordings in Shank1−/− mice, gephyrin immunoblot

    PMID:25816842

    Open questions at the time
    • Mechanism linking SHANK1 loss to reduced gephyrin not defined
    • Behavioral consequence of E/I shift not assessed here
  11. 2021 Medium

    Truncating variant analysis answered why human mutations are pathogenic: stable truncated protein loses Homer1 binding and fails to localize to synapses.

    Evidence NMD knock-in lines, HEK293 binding assays, neuronal localization imaging

    PMID:34113010

    Open questions at the time
    • Synaptic functional deficit of mislocalized protein not measured
    • Dominant vs loss-of-function mechanism not resolved
  12. 2022 High

    ASD missense knock-in models identified mGluR1–IP3R1–calcium signaling downregulation as the convergent pathological mechanism, with subsequent independent confirmation.

    Evidence R874H and P1812L knock-in mice with electrophysiology, EM, and pathway immunoblotting

    PMID:35388181 PMID:37880287

    Open questions at the time
    • Molecular link from SHANK1 to mGluR1 signaling not biochemically mapped
    • Whether scaffolding loss or gain drives the deficit unresolved
  13. 2022 Medium

    Identification of a SHANK1–MDM2–Klotho ternary complex revealed a non-neuronal role for SHANK1 in scaffolding ubiquitination of a tumor suppressor.

    Evidence Co-IP, ubiquitination assay, knockdown/overexpression in NSCLC cells, xenograft

    PMID:35468874

    Open questions at the time
    • Direct vs bridged interactions within the complex not separated
    • Domain of SHANK1 mediating MDM2/Klotho binding not mapped
  14. 2025 Medium

    USP18 deubiquitination and EZH2/H3K27me3 silencing answered how SHANK1 protein and transcript levels are set in cancer, with functional consequences for drug resistance and Wnt signaling.

    Evidence Co-IP and ubiquitination assays for USP18; promoter ChIP and rescue for EZH2; β-catenin and tumor growth readouts

    PMID:40096187 PMID:41274253

    Open questions at the time
    • How SHANK1 suppresses Wnt/β-catenin mechanistically not defined
    • Relationship between cancer and neuronal SHANK1 functions unclear
  15. 2025 Medium

    PKA/CREB was shown to control SHANK1 transcription, defining an upstream signaling input that couples activity to scaffold abundance and synaptic function.

    Evidence PKA modulation, CREB S133A/S133D mutagenesis, RNA-seq, dendritic morphology and electrophysiology in rat hippocampus

    PMID:40574425

    Open questions at the time
    • Whether CREB binds the SHANK1 promoter directly not shown
    • Physiological stimuli driving this axis not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SHANK1 mechanistically links its scaffold to mGluR1 signaling, and how local translational and transcriptional controls are integrated by synaptic activity in vivo, remain unresolved.
  • No biochemical bridge from SHANK1 to mGluR1/IP3R1 mapped
  • Activity-dependent coupling of transport, uORF, and PKA/CREB control not integrated
  • Unified explanation for neuronal vs oncogenic roles absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0005198 structural molecule activity 2 GO:0008092 cytoskeletal protein binding 1
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-162582 Signal Transduction 2
Partners
BETAPIXCIRL1FMRPGKAP/SAPAPHOMER1IRSP53MDM2USP18
Complex memberships
SHANK1-MDM2-Klotho ternary complexpostsynaptic density (PSD)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 Synamon (SHANK1) was identified as a novel neuronal protein that interacts with GKAP/SAPAP/DAP via its PDZ domain (middle region). It was co-immunoprecipitated with SAPAP from rat crude synaptosomes and co-localized with SAPAP in cultured rat hippocampal neurons, placing it in the PSD scaffold complex. Yeast two-hybrid screening, co-immunoprecipitation from rat synaptosomes, co-localization in primary cultured neurons The Journal of biological chemistry High 10488079
2000 The PDZ domain of SHANK1 (ProSAP/SSTRIP) directly interacts with the C-termini of CIRL1 and CIRL2 (calcium-independent receptors for alpha-latrotoxin) in vitro; in vivo, only CIRL1 (not CIRL2) was co-immunoprecipitated with ProSAP1 from solubilized rat brain membranes. Both proteins are enriched in the postsynaptic density fraction. Yeast two-hybrid, in vitro binding assay, co-immunoprecipitation from rat brain membrane fractions, subcellular fractionation The Journal of biological chemistry High 10964907
2002 The PDZ domain of Shank1 from rat brain was crystallized (peptide-free at 1.8 Å and in complex with the C-terminal octapeptide of GKAP at 3.2 Å resolution), establishing the structural basis for GKAP binding via the PDZ domain. X-ray crystallography Acta crystallographica. Section D, Biological crystallography Medium 12136153
2002 The proline-rich region of Shank1 (residues 911–940) interacts with the SH3 domain of IRSp53 via overlay assay. IRSp53 co-precipitates with Shank1 from transfected HEK cells in a cdc42-regulated manner, linking Shank1 to the small G-protein cdc42 pathway. Co-expression of Shank1 with IRSp53 prevents IRSp53 targeting to filopodia. Yeast two-hybrid, overlay assay, co-immunoprecipitation from HEK293 cells, co-expression/localization assay Molecular and cellular neurosciences Medium 12504591
2004 A 200-nucleotide dendritic targeting element (DTE) in the 3′ UTR of Shank1 mRNA was identified by reporter assays in hippocampal neurons; Shank1 and Shank3 (but not Shank2) mRNAs are present in the molecular layers of the hippocampus consistent with dendritic localization, and Shank1/Shank2 transcripts are in dendritic fields of Purkinje cells. In situ hybridization, reporter transcript expression in hippocampal neurons Molecular and cellular neurosciences Medium 15121189
2008 Shank1 knockout mice show altered PSD protein composition, reduced dendritic spine size, smaller and thinner PSDs, and weaker basal synaptic transmission, establishing that Shank1 is required for normal synapse structure and synaptic strength in vivo. Genetic knockout (Shank1−/−), electron microscopy of PSD, electrophysiology, immunoblot of PSD fractions The Journal of neuroscience High 18272690
2009 Shank1 mRNA granules undergo saltatory microtubule-dependent transport in dendrites involving the kinesin motor KIF5C and the KIF5-associated RNA-binding protein staufen1, as shown by dominant-negative interference. Translation of Shank1 mRNA is strongly inhibited by a GC-rich 5′ UTR; internal ribosome entry sites are absent, distinguishing its translational regulation from other dendritic mRNAs. Live cell imaging, dominant-negative protein expression, co-fractionation of brain mRNPs with KIF5C cargo-binding domain, reporter assays Traffic (Copenhagen, Denmark) Medium 19416473
2011 Crystal structure of the Shank1 PDZ domain in complex with the βPIX C-terminal pentapeptide (DETNL) at 2.3 Å resolution revealed a large hydrophobic pocket accommodating variable P0 residues, an invariant H-bond between His735 and Ser/Thr at P−2, and flexible loops enabling structural plasticity for binding diverse ligands. X-ray crystallography at 2.3 Å, structural modeling of additional PDZ–peptide complexes Biochemical and biophysical research communications High 21376703
2014 FMRP binds two stable intramolecular G-quadruplex structures in the Shank1 mRNA 3′-UTR with high affinity both in vitro and in vivo; FMRP S500D phospho-mimic also binds these structures, identifying G-quadruplex motifs as structural elements mediating FMRP regulation of Shank1 mRNA. Biophysical assays (in vitro binding), in vivo interaction assays, G-quadruplex structural analysis RNA biology Medium 25692235
2014 Translation of Shank1 mRNA requires a non-canonical ACG start codon upstream of the main ORF: mutation of this ACG nearly abolishes translation initiation at AUG+1, revealing a novel translational control mechanism where a non-canonical uORF is required for Shank1 synthesis despite a highly structured 5′ UTR. Reporter assays with mutagenesis in heterologous cells PloS one Medium 24533096
2015 Shank1 protein is highly localized in parvalbumin-expressing (PV+) fast-spiking inhibitory interneurons in the hippocampus. Loss of Shank1 in these neurons reduces excitatory synaptic inputs and inhibitory synaptic outputs to pyramidal neurons, and decreases gephyrin expression, shifting the excitatory/inhibitory balance in hippocampal CA1. Immunofluorescence localization, electrophysiology (miniature EPSCs/IPSCs in Shank1−/− mice), immunoblot for gephyrin The European journal of neuroscience High 25816842
2021 De novo truncating variants in SHANK1 produce stable transcripts (escaping NMD) but cause complete loss of Homer1 binding (which requires the SHANK1 C-terminus). Truncated SHANK1 expressed in neurons shows dispersed localization in the spine and dendritic shaft rather than normal synaptic targeting, indicating impaired synaptic localization. Knock-in cell lines for NMD assessment, HEK293 expression, hippocampal neuron expression/immunofluorescence localization Genetics in medicine Medium 34113010
2022 A recurrent ASD missense mutation R874H in Shank1 causes downregulation of mGluR1-IP3R1-calcium signaling in frontal cortex, hippocampus, and cerebellar cortex in knock-in mice, with accompanying decreased spine size, reduced spine density, abnormal PSD morphology, and impaired hippocampal LTP and basal excitatory transmission. Knock-in mouse model, structural MRI, electrophysiology (LTP, basal excitatory transmission), electron microscopy (spine/PSD morphology), western blot for mGluR1/IP3R1/calcium signaling pathway components Molecular psychiatry High 35388181
2022 SHANK1 interacts with the E3 ubiquitin ligase MDM2 and the tumor suppressor Klotho, forming a ternary complex that enhances MDM2-mediated ubiquitination and proteasomal degradation of Klotho in non-small cell lung cancer cells. Co-immunoprecipitation, ubiquitination assay, overexpression/knockdown in NSCLC cells, mouse xenograft model Cell death & disease Medium 35468874
2023 A second ASD-associated Shank1 knock-in mutation (P1812L) also causes downregulation of mGluR1 signaling and dendritic spine structural abnormalities, corroborating that mGluR1-mediated signaling dysfunction is a convergent mechanism in Shank1-related ASD pathology. Knock-in mouse model, electrophysiology, western blot for mGluR1 and associated signals, electron microscopy of dendritic spines/PSDs Translational psychiatry Medium 37880287
2024 X-ray co-crystal structure of the SHANK1 PDZ domain with an internal short linear motif (SLiM) peptide Ac-EESTSFQGP-CONH2 at atomic resolution revealed that the PDZ backbone adopts an orientation overlapping with canonical C-terminal PBM binding, with flexible loops reorganizing to accommodate the internal ligand; the terminal Gly and Pro residues do not participate in contact with the domain. X-ray crystallography, fluorescence anisotropy competition assay The Biochemical journal High 38899489
2025 USP18 deubiquitinates SHANK1 and stabilizes its protein expression in paclitaxel-resistant NSCLC cells; Co-IP validated the USP18–SHANK1 interaction, and silencing USP18 reduced SHANK1 levels, promoted paclitaxel sensitivity, suppressed glycolysis, and induced apoptosis, while SHANK1 overexpression reversed these effects. Co-immunoprecipitation, cellular ubiquitination assay, siRNA knockdown, overexpression rescue, in vivo xenograft Journal of biochemical and molecular toxicology Medium 40096187
2025 PKA/CREB signaling controls SHANK1 transcription: pharmacological inhibition of PKA/CREB reduces SHANK1 expression and impairs dendritic structure and synaptic function; PKA activation restores CREB activity and SHANK1 levels. A CREB S133A mutant blocks PKA-induced SHANK1 upregulation, while constitutively active CREB S133D prevents SHANK1 downregulation, demonstrating CREB is essential for SHANK1 regulation. Pharmacological PKA inhibition/activation, CREB mutagenesis (S133A/S133D), RNA sequencing, western blot, dendritic morphology analysis, electrophysiology in rat hippocampus Advanced science Medium 40574425
2025 EZH2 epigenetically silences SHANK1 via H3K27 trimethylation at its promoter in glioblastoma stem cells; pharmacological or genetic EZH2 inhibition restores SHANK1 expression. SHANK1 overexpression inhibits Wnt/β-catenin signaling by reducing β-catenin levels, impairing GSC self-renewal and tumor growth. ChIP for H3K27me3 at SHANK1 promoter, EZH2 inhibition (pharmacological and genetic), SHANK1 overexpression, β-catenin reporter/western blot, in vivo tumor growth assay, multiplex immunofluorescence of GBM tissue Biochemical and biophysical research communications Medium 41274253
2025 Disease-associated missense mutations in the Shank1 PDZ domain generally weaken binding to partner peptides in a partner-specific manner dependent on dynamic rearrangements; notably the R736Q mutant has increased thermal stability and binds the GKAP peptide with higher affinity than wild type, demonstrating that mutation effects on ligand binding are highly context-dependent. Experimental binding assays (fluorescence anisotropy), thermal stability measurements, molecular dynamics simulations bioRxivpreprint Medium

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Smaller dendritic spines, weaker synaptic transmission, but enhanced spatial learning in mice lacking Shank1. The Journal of neuroscience : the official journal of the Society for Neuroscience 291 18272690
2012 SHANK1 Deletions in Males with Autism Spectrum Disorder. American journal of human genetics 262 22503632
2011 Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior. PloS one 168 21695253
2004 Differential expression and dendritic transcript localization of Shank family members: identification of a dendritic targeting element in the 3' untranslated region of Shank1 mRNA. Molecular and cellular neurosciences 113 15121189
1999 Synamon, a novel neuronal protein interacting with synapse-associated protein 90/postsynaptic density-95-associated protein. The Journal of biological chemistry 79 10488079
2000 The calcium-independent receptor for alpha-latrotoxin from human and rodent brains interacts with members of the ProSAP/SSTRIP/Shank family of multidomain proteins. The Journal of biological chemistry 77 10964907
2002 The insulin receptor substrate IRSp53 links postsynaptic shank1 to the small G-protein cdc42. Molecular and cellular neurosciences 75 12504591
2014 Repetitive behaviors in the Shank1 knockout mouse model for autism spectrum disorder: developmental aspects and effects of social context. Journal of neuroscience methods 63 24820912
2014 FMRP interacts with G-quadruplex structures in the 3'-UTR of its dendritic target Shank1 mRNA. RNA biology 55 25692235
2015 Shank1 regulates excitatory synaptic transmission in mouse hippocampal parvalbumin-expressing inhibitory interneurons. The European journal of neuroscience 52 25816842
2009 Shank1 mRNA: dendritic transport by kinesin and translational control by the 5'untranslated region. Traffic (Copenhagen, Denmark) 35 19416473
2013 Chronic morphine exposure and its abstinence alters dendritic spine morphology and upregulates Shank1. Neurochemistry international 29 23538264
2022 A recurrent SHANK1 mutation implicated in autism spectrum disorder causes autistic-like core behaviors in mice via downregulation of mGluR1-IP3R1-calcium signaling. Molecular psychiatry 26 35388181
2017 Aberrant cognitive phenotypes and altered hippocampal BDNF expression related to epigenetic modifications in mice lacking the post-synaptic scaffolding protein SHANK1: Implications for autism spectrum disorder. Hippocampus 25 28500650
2021 Correlation of distinct behaviors to the modified expression of cerebral Shank1,3 and BDNF in two autistic animal models. Behavioural brain research 24 33577886
2011 The structural flexibility of the shank1 PDZ domain is important for its binding to different ligands. Biochemical and biophysical research communications 21 21376703
2017 Behavioral phenotypes and neurobiological mechanisms in the Shank1 mouse model for autism spectrum disorder: A translational perspective. Behavioural brain research 20 28963042
2010 Loose ligation of the rat sciatic nerve elicits early accumulation of Shank1 protein in the post-synaptic density of spinal dorsal horn neurons. Pain 19 20171009
2015 Deletion of Shank1 has minimal effects on the molecular composition and function of glutamatergic afferent postsynapses in the mouse inner ear. Hearing research 18 25637745
2014 A non-canonical initiation site is required for efficient translation of the dendritically localized Shank1 mRNA. PloS one 15 24533096
2021 Truncating variants in the SHANK1 gene are associated with a spectrum of neurodevelopmental disorders. Genetics in medicine : official journal of the American College of Medical Genetics 14 34113010
2022 SHANK1 facilitates non-small cell lung cancer processes through modulating the ubiquitination of Klotho by interacting with MDM2. Cell death & disease 13 35468874
2015 SHANK1 and autism spectrum disorders. Science China. Life sciences 12 26335738
2019 SHANK1 polymorphisms and SNP-SNP interactions among SHANK family: A possible cue for recognition to autism spectrum disorder in infant age. Autism research : official journal of the International Society for Autism Research 11 30629339
2018 Neocortical SHANK1 regulation of forebrain dependent associative learning. Neurobiology of learning and memory 7 30053575
2017 SHANK1 is differentially expressed during development in CA1 hippocampal neurons and astrocytes. Developmental neurobiology 7 29218848
2020 The roles of SHANK1 in the development of colon cancer. Cell biochemistry and function 6 32356303
2018 Reduced Efficacy of d-Amphetamine and 3,4-Methylenedioxymethamphetamine in Inducing Hyperactivity in Mice Lacking the Postsynaptic Scaffolding Protein SHANK1. Frontiers in molecular neuroscience 6 30505269
2022 Suv39h1 regulates memory stability by inhibiting the expression of Shank1 in hippocampal newborn neurons. The European journal of neuroscience 5 35181969
2025 USP18 Confers Paclitaxel Resistance in Non-Small Cell Lung Cancer by Stabilizing SHANK1 Expression Via Deubiquitination. Journal of biochemical and molecular toxicology 4 40096187
2024 Biophysical and structural analyses of the interaction between the SHANK1 PDZ domain and an internal SLiM. The Biochemical journal 4 38899489
2023 Downregulation of mGluR1-mediated signaling underlying autistic-like core symptoms in Shank1 P1812L-knock-in mice. Translational psychiatry 3 37880287
2021 Case Report: Lennox-Gastaut Epileptic Encephalopathy Responsive to Cannabidiol Treatment Associated With a Novel de novo Mosaic SHANK1 Variant. Frontiers in genetics 3 34912368
2002 Crystallization and preliminary X-ray crystallographic studies of the PDZ domain of Shank1 from Rattus norvegicus. Acta crystallographica. Section D, Biological crystallography 3 12136153
2025 Long Term High-Salt Diet Induces Cognitive Impairments via Down-Regulating SHANK1. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2 40574425
2024 Ablation of Shank1 Protects against 6-OHDA-induced Cytotoxicity via PRDX3-mediated Inhibition of ER Stress in SN4741 Cells. CNS & neurological disorders drug targets 2 36797610
2026 Discovery of SHANK1-PDZ Peptide-Fragment Inhibitors Using a Dynamic Ligation Screening Strategy. Biochemistry 0 41944827
2025 SHANK1 is epigenetically silenced by EZH2 and suppresses Wnt/β-catenin signaling to inhibit glioblastoma stem cell maintenance. Biochemical and biophysical research communications 0 41274253
2024 Chronic Catatonia in an Individual With a De Novo Missense SHANK1 Variant. American journal of medical genetics. Part A 0 39569511

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