Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of CaMKII splice variants expressed in the human hippocampus

ABSTRACT: Purpose: The goal of this study was to use deep sequencing to identify all splice variants of Calcium/calmodulin-dependent kinase II (CaMKII) expressed in the human hippocampus. Methods: Transcripts of CaMKII-encoding genes (CAMK2A, CAMK2B, CAMK2G, and CAMK2D) were sub-amplified by PCR from total RNA extracted from human hippocampal tissue samples from 3 donors. Illumina sequencing libraries were constructed by PCR from these initial pools of amplicons and sequenced on an Illumina MiSeq instrument. Sequencing reads passing quality controls were clustered on the basis of sequence identity or near-identity. Consensus sequences of clusters were mapped with known exons of CaMKII genes to identify the splice variant represented by each cluster. Donor 1 replicate 2, Donor 2, and Donor 3 libraries from genes CAMK2B, CAMK2G, and CAMK2D were first sequenced on a MiSeq Nano flow cell, then re-pooled for read balancing and sequenced again of a full-size MiSeq flow cell. For each library, reads from Nano and full-size flow cells were combined for subsequent analysis. Results: We perfomed the first comprehensive survey of CaMKII transcripts expressed in individual tissue samples (human hippocampus). We detected a total of 79 splice variants of the four human CaMKIIs: CaMKIIα (3), CaMKIIβ (30), CaMKIIγ (24), and CaMKIIδ (22), across tissue samples from 3 donors. This represents the vast majority of possible in-frame CaMKII splice variants (Sloutsky and Stratton, European Journal of Neuroscience, 2020; https://doi.org/10.1111/ejn.14761).

ORGANISM(S): Homo sapiens

PROVIDER: GSE154030 | GEO | 2020/07/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CaM Kinase II mediates maladaptive post-infarct remodeling but not acute myocardial ischemia/reperfusion injury

Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIδC was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed nor in conditional CaMKIIδ/γ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling.

2014-09-08 | GSE58486 | GEO

CaM Kinase II mediates maladaptive post-infarct remodeling but not acute myocardial ischemia/reperfusion injury

Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIÎ´C was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIÎ´-deficient mice, CaMKIIÎ´-deficient mice in which the splice variants CaMKIIÎ´B and C were re-expressed nor in conditional CaMKIIÎ´/Î³ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling. We analysed 6 groups in total: 3 groups from wild-type control animals and 3 groups from CaMKII delta/gamma double-KO mice. Sham operated animals served as controls in both wild-type and KO animal groups. 2 different time points in ischia/reperfusion operated animals were investigated: 1 day and 5 days post-surgery.

2014-09-08 | E-GEOD-58486 | biostudies-arrayexpress

Identification of CaMKII splice variants expressed in the human hippocampus

Project description:Identification of CaMKII splice variants expressed in the human hippocampus

| PRJNA644901 | ENA

Branch point evolution controls species-specific alternative splicing and regulates long term potentiation

Project description:Regulation and functionality of species-specific alternative splicing has remained enigmatic for many years. Calcium/calmodulin-dependent protein kinase IIβ (CaMKIIβ) is expressed in several splice variants and plays a key role in learning and memory. Here, we identify and characterize several primate-specific CAMK2B splice isoforms, which show altered kinetic properties and changes in substrate specificity. Furthermore, we demonstrate that primate-specific Camk2β alternative splicing is achieved through branch point weakening during evolution. We show that reducing branch point and splice site strength during evolution globally renders constitutive exons alternative, thus providing a paradigm for cis-directed species-specific alternative splicing regulation. Using CRISPR/Cas9 we introduced the weaker human branch point into the mouse genome, resulting in human-like CAMK2B splicing in the brain of mutant mice. We observe a strong impairment of long-term potentiation in CA3-CA1 synapses of mutant mice, thus connecting branch point-controlled, species-specific alternative splicing with a fundamental function in learning and memory.

2022-12-19 | PXD035346 | Pride

Branch point evolution controls species-specific alternative splicing and regulates long term potentiation

2022-12-02 | GSE208181 | GEO

Targeted sequencing of 49 primary medulloblastoma samples using Illumina TruSight Tumor 15 assay

Project description:The mutation status of TP53 was analyzed by next generation sequencing using the Illumina TruSight Tumor (TST) 15 assay (Illumina) at the Molecular Pathology Center of the Jewish General Hospital (Montreal, QC, Canada). The CAP-compliant clinically validated TST15 assay was performed as per supplier's instruction with 10 ng DNA input. Libraries were sequenced on a MiSeq with a v3 flow cell (Illumina). Data was analyzed with a clinically validated pipeline (NextGene, SoftGenetics) and variants were annotated in Geneticist Assistant (SoftGenetics). The IARC TP53 database version R18 was consulted for the molecular interpretation of TP53 variants (www.p53.iarc.fr).

2018-03-20 | E-MTAB-6546 | biostudies-arrayexpress

Effect specific ablation of the NCoR corepressor delta and omega splice-variants on liver gene expression

Project description:Knockin mice were created that contained a point mutation that elminated the requisite GT in the 5' donor site of each of the NCoRω or NCoRδ splice variants, thus preventing splicing at that site and forcing splicing of the reciprocal splice variant.

2020-09-11 | GSE157761 | GEO

Alterations in liver and epididymal white adipose tissue (eWAT) gene expression in mice with a global ablation of the NcoRω splice isoform of the corepressor Ncor1

Project description:A knockin mouse line created that contains a point mutation that elminates the requisite GT in the 5' donor site of each of the NCoRω splice variants, thus preventing splicing at that site and forcing splicing of the reciprocal NcoRδ splice variant.

2020-10-27 | GSE160121 | GEO

Nanopore PCR-free direct cDNA sequencing of human kidney tissue

Project description:Anonynous donor kidneys were sequenced using the Nanopore long-read direct cDNA sequencing kit (SQK-DCS109) and R9.4.1 flow cells.

2024-11-10 | GSE281264 | GEO

Project description:STIM1 splice variants

| PRJNA768993 | ENA