The CCDC55 couples cannabinoid receptor CNR1 to a putative DISC1 schizophrenia pathway

Xie, Jianjun; Gizatullin, Rinat; Vukojević, Vladana; Leopardi, Rosario

doi:10.1016/j.neuroscience.2015.10.012

Cited by 7 publications

(4 citation statements)

References 57 publications

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“…Interestingly, CNR1 has also been linked to cases of complete absence of expressive speech (Poot et al, 2009). CNR1 is functionally linked to the last gene we wish to highlight, namely, DISC1 (Xie et al, 2015). DISC1 encodes a protein involved in neurite outgrowth, cortical development and callosal formation (Brandon and Sawa, 2011; Osbun et al, 2011).…”

Section: Schizophrenia-related Genes and Some Evolutionary Concernsmentioning

confidence: 99%

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Murphy

Benítez‐Burraco

2016

Front. Hum. Neurosci.

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Schizophrenia is characterized by marked language deficits, but it is not clear how these deficits arise from the alteration of genes related to the disease. The goal of this paper is to aid the bridging of the gap between genes and schizophrenia and, ultimately, give support to the view that the abnormal presentation of language in this condition is heavily rooted in the evolutionary processes that brought about modern language. To that end we will focus on how the schizophrenic brain processes language and, particularly, on its distinctive oscillatory profile during language processing. Additionally, we will show that candidate genes for schizophrenia are overrepresented among the set of genes that are believed to be important for the evolution of the human faculty of language. These genes crucially include (and are related to) genes involved in brain rhythmicity. We will claim that this translational effort and the links we uncover may help develop an understanding of language evolution, along with the etiology of schizophrenia, its clinical/linguistic profile, and its high prevalence among modern populations.

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Section: Schizophrenia-related Genes and Some Evolutionary Concernsmentioning

confidence: 99%

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Murphy

Benítez‐Burraco

2016

Front. Hum. Neurosci.

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“…CRIP1a has been linked to neuropathological states such as epilepsy and neurotoxicity in the hippocampus [11,12,13,14], schizophrenia phenotype [15,16], and motor dysfunction and addiction in the striatum [17], making the CRIP1a-CB 1 receptor interaction an accessible target for novel drug design. This review focused on the structural interaction between the CB 1 receptor and its association with CRIP1a.…”

Section: Discussionmentioning

confidence: 99%

“…The purpose of the present review is to describe the unique interactions that CRIP1a can have with the CB 1 receptor to regulate cellular signaling and CB 1 receptor trafficking. Regulation of CB 1 receptor activity by CRIP1a can be investigated at both the functional and structural levels with the goal of designing peptide or small molecule drugs that can selectively target the CRIP1a-CB 1 receptor interaction for therapeutic intervention in the treatment of pain, convulsions [11,12,13,14], schizophrenia [15,16], and neurodegenerative motor disorders [17].…”

Section: Introductionmentioning

confidence: 99%

Cannabinoid Receptor Interacting Protein 1a (CRIP1a): Function and Structure

et al. 2019

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Cannabinoid receptor interacting protein 1a (CRIP1a) is an important CB1 cannabinoid receptor-associated protein, first identified from a yeast two-hybrid screen to modulate CB1-mediated N-type Ca2+ currents. In this paper we review studies of CRIP1a function and structure based upon in vitro experiments and computational chemistry, which elucidate the specific mechanisms for the interaction of CRIP1a with CB1 receptors. N18TG2 neuronal cells overexpressing or silencing CRIP1a highlighted the ability of CRIP1 to regulate cyclic adenosine 3′,5′monophosphate (cAMP) production and extracellular signal-regulated kinase (ERK1/2) phosphorylation. These studies indicated that CRIP1a attenuates the G protein signaling cascade through modulating which Gi/o subtypes interact with the CB1 receptor. CRIP1a also attenuates CB1 receptor internalization via β-arrestin, suggesting that CRIP1a competes for β-arrestin binding to the CB1 receptor. Predictions of CRIP1a secondary structure suggest that residues 34-110 are minimally necessary for association with key amino acids within the distal C-terminus of the CB1 receptor, as well as the mGlu8a metabotropic glutamate receptor. These interactions are disrupted through phosphorylation of serines and threonines in these regions. Through investigations of the function and structure of CRIP1a, new pharmacotherapies based upon the CRIP-CB1 receptor interaction can be designed to treat diseases such as epilepsy, motor dysfunctions and schizophrenia.

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“…Based on this structure, NSrp70 belongs to the SR protein family and plays an important role in alternative splicing [9]. To date, functional studies into NSrp70 have focused on schizophrenia [10], embryonic development [11], and adult acute leukemia [12]. However, the function of NSrp70 in carcinoma remains unknown.…”

Section: Introductionmentioning

confidence: 99%

NSrp70 suppresses metastasis in triple-negative breast cancer by modulating Numb/TβR1/EMT axis

Zhao

Sun

Zhao

et al. 2021

Preprint

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Metastasis is a major cause of death in individuals suffering from triple-negative breast cancer. Alternative splicing of mRNA precursor allows cancer cells to create different protein isoforms which may promote metastasis. Quantitative proteomic analysis of primary and metastatic breast cancer cells revealed that nuclear speckle-related protein 70 (NSrp70) was significantly downregulated in highly metastatic cells. Downregulation of NSrp70 promoted the migration and invasion of breast cancer cells in vitro and in vivo. Mechanistically, we found that NSrp70 inhibited the skipped exon alternative splicing of NUMB, promoted the degradation of TGF-beta receptor 1(TβR1) through lysosome pathway, and regulated TGFβ/SMAD-mediated epithelial-mesenchymal transition (EMT) phenotype in breast cancer cells. Furthermore, high NSrp70 expression correlated with better prognosis in breast cancer patients. Our findings revealed that splicing regulator NSrp70 may serve as a metastasis suppressor.

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The CCDC55 couples cannabinoid receptor CNR1 to a putative DISC1 schizophrenia pathway

Cited by 7 publications

References 57 publications

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Bridging the Gap between Genes and Language Deficits in Schizophrenia: An Oscillopathic Approach

Cannabinoid Receptor Interacting Protein 1a (CRIP1a): Function and Structure

NSrp70 suppresses metastasis in triple-negative breast cancer by modulating Numb/TβR1/EMT axis

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