PICK1 antibody
- Known as:
- PICK1 (anti-)
- Catalog number:
- orb101611
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- PICK1 antibody
Related genes to: PICK1 antibody
- Gene:
- PICK1 NIH gene
- Name:
- protein interacting with PRKCA 1
- Previous symbol:
- PRKCABP
- Synonyms:
- dJ1039K5, MGC15204
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-19
- Date modifiied:
- 2014-11-19
Related products to: PICK1 antibody
Related articles to: PICK1 antibody
- Palmitoylation has been implicated in learning and memory processes, yet its precise role and underlying mechanisms remain poorly understood. Here, we report a novel role of palmitoylation in regulating amygdalar synaptic plasticity and fear memory, involving the regulation of palmitate cycling on PSD-95. Using a series of multi-methodological experiments, we demonstrated that conditioned fear learning impairs amygdalar metaplasticity-an effect not observed in the hippocampus. Furthermore, PSD-95 recruits LTP-like mechanisms at lateral amygdala (LA) synapses, and its palmitoylation is critically involved in fear memory expression. Notably, PSD-95 palmitoylation contributes to the occlusion of LA-LTP following fear conditioning. Mechanistically, DHHC2 drives PSD-95 palmitoylation and modulates LA synaptic plasticity following fear conditioning, whereas PICK1 facilitates the activity-dependent trafficking of DHHC2 to PSD-95 at synapses. Collectively, these findings highlight the PICK1-DHHC2-PSD-95 pathway as a critical regulator of learning-dependent metaplasticity in the LA, which occludes further HFS-induced LTP while promoting fear memory expression. - Source: PubMed
Publication date: 2026/07/06
Shen Zu-ChengWeng Yu-XuanXia Zhi-XuanZhao Yue-LingDing Qian-QianWang Si-YingCao TingChen Xuan-YingTao Wu-ChengLin ShenChen ZhouLuo Yi-Xiao - Chronic neuropathic pain's impact, persistence, and limited treatments render it relevant for gene therapy. Here, we describe the development and application of self-assembling dimeric peptide inhibitors of the pain-associated scaffolding protein PICK1 (protein interacting with C-kinase 1), delivered by adeno-associated viral (AAV) vectors. In mice, these peptides prevent mechanical allodynia in inflammatory and neuropathic pain models and reverse neuropathic pain for up to 1 year. Targeting somatosensory pathways relieves pain without overt side effects, while selective transduction of dorsal root ganglion (DRG) neurons is sufficient to provide pain relief. Using proteomic and phosphoproteomic analysis of DRG tissue, we identify regulation of protein kinase C alpha (PRKCA) as a candidate that potentially shapes this pain-relieving phenotype. We finally confirm PICK1 expression and peptide target engagement in human donor tissue, supporting the potential of AAV-encoded PICK1 inhibitors as a clinically meaningful strategy for neuropathic pain conditions. - Source: PubMed
Publication date: 2026/05/13
Noes-Holt GithJensen Kathrine LComaposada-Baró RaquelJager Sara ERichner MetteGoddard Carolyn MKowenicki Marco B KSivertsen LineJiménez-Fernández LucíaAndersen Rita CLilja Jamila HLarsen Andreas HBoesgaard Sofie PHouser Grace AChristensen Nikolaj RMarino AntonioTappe-Theodor AnkeWierer MichaelVægter Christian BKuner RohiniMadsen Kenneth LSørensen Andreas T - Glutamate metabotropic receptors (mGluRs) and their molecular partners at the postsynaptic density (PSD) represent a highly dynamic molecular hub that integrates multiple neurotransmitter signals and regulates synaptic plasticity and metaplasticity, which are putatively involved in the pathophysiology of psychiatric illnesses, including schizophrenia. Group I mGluRs (mGluR1 and mGluR5) interact with PSD adaptor and scaffolding proteins, such as Homer, Shank, Norbin, and PICK1, as well as intracellular downstream effectors, creating a molecular network that resembles a Lego-like structure, where modular protein interactions fine-tune glutamatergic transmission. Evidence from preclinical research indicates that dysregulation of mGluR expression and function, along with disrupted PSD protein expression, may contribute to the pathophysiology of schizophrenia by altering glutamatergic neurotransmission and synaptic stability. Antipsychotic mechanisms of action may involve, at least in part, the modulation of mGluR activity mediated through PSD proteins. Notably, novel agents that enhance spinogenesis by acting at the level of PSD proteins, such as SPG302, may open promising avenues for therapeutics aimed at restoring synaptic integrity. While Group I mGluRs dominate postsynaptic regulation, Group II (mGluR2/3) and III (mGluR4/6/7/8) receptors -primarily presynaptic- inhibit neurotransmitter release and plasticity, offering complementary therapeutic avenues. Emerging strategies, such as allosteric modulators of mGluRs, aim to rebalance synaptic signaling in treatment-resistant schizophrenia. This review synthesizes how PSD proteins and mGluRs interact in schizophrenia, exploring their potential as druggable targets for novel therapies. - Source: PubMed
Publication date: 2026/02/19
Barone AnnaritaVellucci LiciaNasti AnitaMazza BenedettaIannotta FedericaIasevoli Felicede Bartolomeis Andrea - AMPA receptors are a type of ionotropic glutamate receptor that is important for fast excitatory neurotransmission. healthy brain function. Glutamate signaling is regulated, in part, by the trafficking of glutamate receptors in and out of the synapse. Multiple different trafficking and auxiliary proteins govern this process. Disruptions in this trafficking are linked to various psychiatric diseases, including schizophrenia, major depressive disorder. Glutamate, the primary excitatory neurotransmitter, is crucial for synaptic plasticity and and substance use disorder. Moreover, the incidence and symptomology of these psychiatric diseases impact males and females differently. Despite these epidemiological sex differences, very little research has considered the influence of biological sex on glutamatergic trafficking. Here, we review the current literature on glutamate trafficking proteins for AMPA receptors, most of which have mainly utilized male rodents and cell cultures. The following proteins were explored for AMPA receptors: GRIP, PICK1, NSF, SAP97, AKAP79/150, Protein 4.1 N, and PSD-95. Overall, these studies revealed that our fundamental understanding of glutamate trafficking is based almost completely on studies performed in male animals, and the assumption that the same mechanisms govern AMPAR trafficking in females may not be correct. To fully grasp how these proteins are impacted in disease models, it's crucial to first understand the baseline sex differences. This is especially important if we want to investigate new research avenues for treating diseases that affect each sex differently. - Source: PubMed
Publication date: 2026/02/13
Roberts Mia YBriand Lisa A - - Source: PubMed
Publication date: 2026/02/06
Hendrix EmilyHe Yi