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PubMed2025

Loss of responses to odorants and pheromones in mPRγ (paqr5b)-knockout zebrafish.

In our previous study, we generated a membrane-type progesterone receptor γ (paqr5b) knockout zebrafish line. Knocking out paqr5b by genome editing resulted in the loss of neurons in the olfactory rosette (OR). These findings indicated that Paqr5b plays an essential role in the formation of olfactory neurons. In this study, we investigated the extent to which paqr5b-/- fish lacking olfactory neurons retain their sense of smell. We used a reported tank for zebrafish olfactory analysis with a dividing plate in the middle. The tank was divided into three zones: the right zone, where test substances were added; the neutral zone; and the left zone. The fish were released into the neutral zone at the beginning of each test, the chemical was added to the corner of the right zone, and a 3-min video was taken to track the movements of the fish. The video was then played back, and the time spent in the three zones was counted manually. Both male and female paqr5b+/+ and paqr5b-/- zebrafish were separately analyzed for time spent in the three zones after exposure to ATP, cadaverine, and the pheromone 17α,20β-dihydroxy-4-pregnen-3-one (DHP). Both male and female paqr5b+/+ zebrafish were strongly attracted to ATP and stayed in the right zone for approximately 2 min (67%). In addition, paqr5b+/+ zebrafish avoided cadaverine and stayed longer in the left zone than in any other zone. In contrast, paqr5b-/- zebrafish stayed in all three zones for approximately the same amount of time, even after exposure to ATP and cadaverine. The paqr5b+/+ fish were attracted to DHP and stayed in the right zone longer. Paqr5b-/- zebrafish of either sex were not reactive to DHP exposure. These results showed that paqr5b-/- zebrafish lacking olfactory neurons lost responsiveness to odorants and pheromones.

Animals↗
PubMed2026

Age-dependent reorganization of behavioral and striatal function in Cntnap2 knockout mice.

Autism spectrum disorder (ASD) is characterized by persistent deficits in social communication and the presence of restricted and repetitive behaviors. While ASD has a neurodevelopmental origin, it remains a lifelong condition, yet little is known about how its behavioral and neural features evolve across adulthood. Here, we investigated behavioral, synaptic, and structural alterations across the transition from early to mature adulthood in Cntnap2 knockout mice, a widely used model of ASD. Using a longitudinal behavioral approach combined with electrophysiological recordings and morphological analysis, we show that KO mice exhibit increased stereotyped and repetitive behaviors and reduced exploratory activity at both ages. However, detailed analysis of behavioral patterns revealed age-dependent differences, with early adult KO mice displaying increased behavioral persistence that later evolved into distinct patterns of behavioral sequences. These behavioral changes were associated with alterations in inhibitory synaptic transmission in the dorsolateral striatum (DLS), including changes in spontaneous inhibitory postsynaptic current (sIPSC) frequency and temporal structure. In parallel, mature adult KO mice showed structural remodeling of spiny projection neurons, characterized by increased distal dendritic arborization and age-dependent organization of dendritic spines. Together, our findings demonstrate that ASD-related alterations are not static but evolve across adulthood, revealing a multi-level reorganization of behavioral, synaptic, and structural features. These results highlight the importance of considering adulthood stages in ASD and provide new insights into the dynamic nature of the condition.

Animals↗
PubMed2026

CRISPR/Cpf1-mediated knockout of FLG in human induced pluripotent stem cells generates a model for studying epidermal barrier dysfunction.

Loss of filaggrin (FLG) function impairs skin barrier formation and contributes to common inflammatory skin diseases. In this study, we established a FLG knockout human induced pluripotent stem cell (iPSC) line based on KOLF2.1 J using CRISPR/Cas12a (Cpf1)-mediated genome editing. A guide RNA targeting exon 2 introduced a homozygous mutation, which was confirmed by sequencing. The edited cells maintained typical pluripotent stem cell morphology, expressed key undifferentiated markers, and retained the ability to differentiate into all three germ layers. Karyotype and copy number variation (CNV) analyses confirmed genomic stability and parental origin; the cells were free of mycoplasma. This cell line enables studies of FLG-associated skin biology and pathology.

Humans↗
PubMed2025

A method for authenticating the fidelity of Cryptococcus neoformans knockout collections.

Gene knockout (KO) strain collections are important tools for discovery in microbiology. Cryptococcus neoformans, a human fungal pathogen, has an available genome-wide gene deletion collection that is widely used by the research community. We uncovered mix-ups in the assembly of the commercially available C. neoformans deletion collection of ~4,700 unique strains acquired by our laboratory. Evidence supporting a mix-up includes RNAseq analysis that identified transcripts for the gene listed as the KO. The mystery was soon solved as this same KO strain lacked RNA transcripts for a different KO strain gene found in the same plate position in an earlier partial KO collection, suggesting a plate swap between two KO collections. Therefore, we developed a quick PCR assay to distinguish the two KO collections based on the size differences between their nourseothricin (NAT)-resistance cassettes, confirmed by genome sequencing. Here, we report that nine of the first 15 plates of the 42-plate our KN99ɑ KO collection had been replaced with the corresponding plates from an earlier partial KO collection. We provide additional evidence that the remaining plates are correct, and the simple authentication method presented here serves as a quick check to identify similar mix-ups in the KO collections.IMPORTANCEGene KO strain collections are important tools for discovery in microbiology. The human fungal pathogen Cryptococcus neoformans has an available genome-wide deletion collection that is widely used by the research community. Here, we report that our KN99ɑ collection is comprised of mixed plates from two independent KO libraries and present a simple authentication method that other investigators can use to distinguish the identities of these KO collections. Above all, this article serves as a reminder to users of the 2015 KO library collection to screen the plates before undertaking large phenotyping experiments.

Cryptococcus neoformans↗
PubMed2026

Disrupted development of the retina in the Ccdc85c knockout rat.

The coiled-coil domain-containing 85c (Ccdc85c) knockout (KO) rat generated by genome editing exhibits hydrocephalus and subcortical heterotopia. In this study, we aimed to further investigate the function of CCDC85C protein in the development of the retina. Expression of CCDC85C, acetylated tubulin, ciliary rootlet coiled-coil protein (CROCC), zonula occludens-1 (ZO-1), glutamine synthetase, and PAX6 were examined immunohistochemically in wild-type F344 rats at embryonic day (ED) 19 and at postnatal days (PNDs) 0, 4, 6, 13, and 20. Immunoelectron microscopy was performed for CCDC85C in the normal rat retina. Retinal lesions in Ccdc85c KO rats were examined using fundus photography, optical coherence tomography (OCT), and histology. In the normal rat retina, CCDC85C was co-localized with ZO-1 in the outer limiting membrane and persistently expressed after ED19. Ultrastructurally, CCDC85C was located between the outer nuclear layer and the inner segments, and showed the same location as the tight junction. In Ccdc85c KO rats, multifocal retinal dysplasia; disarrangement of the inner and outer segments, cilia, and rootlets; and impaired development of Müller cells were observed. In OCT images, Ccdc85c KO rats showed parallel hyperintense striations in the inner nuclear layer, and low reflectivity of the outer limiting membrane and layer of rods and cones. These results suggest that CCDC85C protein is located in the tight junction complex and is involved in retinal layer formation. The Ccdc85c KO rat model provides a novel tool to study retinal development as well as genetic hydrocephalus.

Ccdc85c↗
PubMed2026

Analysis of gene expression changes upon topobexin treatment and TOP2B-knockout in hiPSC-derived cardiomyocytes.

The role of DNA topoisomerase II beta (TOP2B) in cardiomyocyte differentiation is poorly understood. To address this, human induced pluripotent stem cells (hiPSC) were differentiated into cardiomyocytes (CM) that were wild type (WT) or contained a genomic deletion of Topoisomerase 2B (BKO). Both WT and BKO hiPSC could be induced to differentiate into sheets of beating cardiomyocytes. BKO hiPSC take slightly longer to differentiate into sheets of beating CM than WT iPSC. RNA was prepared from both undifferentiated and differentiated WT and BKO hiPSC. RNA-seq was used to examine gene expression changes when the WT and BKO hiPSC were differentiated into CM. Gene expression changes following differentiation of BKO cells were largely similar to those in WT cells. In addition, the differentiated WT CM were treated with dexrazoxane (ICRF-187), a TOP2 catalytic inhibitor that targets both TOP2A and TOP2B, or topobexin, a new TOP2B selective catalytic inhibitor. Topobexin inhibition partially phenocopied a TOP2B deletion and thereby providing an alternative to TOP2B gene knockout in many cell lines. In future, hiPSC derived CM with and without TOP2B and inhibition by topobexin ex vivo CM could be used to study anthracycline-induced cardiotoxicity and to screen for cardioprotectants.

Myocytes, Cardiac↗
PubMed2026

Comparative Proteomic Analysis of the Striatum in Heterozygous and Null DAT Knockout Rats.

Deregulation of striatal neurotransmission is a key pathogenetic mechanism in neurodevelopmental disorders such as attention deficit hyperactivity disorder (ADHD) and autism. In the present study, we applied a proteomic approach to demonstrate shifts in striatal protein expression in rats with heterozygous (DAT-Het) and homozygous (DAT-KO) dopamine transporter (DAT) gene knockouts. These animals model dose-dependent ADHD- and autism-like behaviors, ranging from slightly increased activity and social disturbances in DAT-Het rats to a pronounced phenotype in DAT-KO rats. We revealed pronounced changes in the proteomic profiles of both groups, associated primarily with deregulation of proteins involved in energy and carbon metabolism. Furthermore, we identified changes in vesicular transport proteins specific to DAT-KO and DAT-Het rats. Since these changes involved SNARE complex components, we evaluated SNARE mRNA expression in our models and public transcriptomic data for mouse models of neurodevelopmental disorders, including Mbd5 gene haploinsufficiency and a polygenic model of ADHD. No significant changes in mRNA levels were revealed in any model. Thus, the identified protein expression changes likely depend on post-transcriptional mechanisms. These data suggest a deregulation of metabolism in DAT-Het rats, which becomes more pronounced in DAT-KO rats.

Animals↗
PubMed2026

Tumor-like proliferation of CCM3 knockout endothelial cells: insights from semaxinib treatment and transcriptome profiling of co-cultures.

Cerebral cavernous malformations (CCMs) are vascular lesions associated with severe neurological complications. Increasing evidence suggests that cancer-like mechanisms, like an abnormal expansion of CCM3 knockout (KO) endothelial cells (ECs) in co-culture with wild-type (WT) cells, contribute to lesion formation. Yet, the underlying processes remain poorly understood. Here, we employed a human induced pluripotent stem cell (iPSC)-derived EC co-culture model to screen a cytokine inhibitor library for modulators of this tumor-like behavior. We identified the known VEGFR2 inhibitor semaxinib which selectively suppressed proliferation of WT ECs in co-culture, but not in monoculture. In contrast, CCM3 KO cells maintained their abnormal expansion under semaxinib treatment which was unaffected by modulation of extracellular VEGFA levels. RNA-seq profiling revealed distinct transcriptional responses to semaxinib including extracellular matrix remodeling, stress signaling, and overexpression of growth factors and receptors in CCM3 KO cells, which may contribute to their survival advantage. These findings advance our understanding of the complex interplay between WT and KO cells in CCM pathogenesis and demonstrate that the proliferative advantage of CCM3-deficient cells is not solely driven by CCM3 loss. Finally, our iPSC-based EC co-culture assay provides a scalable platform to study KO/WT interactions and may accelerate the identification of effective therapeutic strategies for CCM disease.

Humans↗
PubMed2024

Activated NAD+ biosynthesis pathway induces olaparib resistance in BRCA1 knockout pancreatic cancer cells.

PARP inhibitors have been developed as anti-cancer agents based on synthetic lethality in homologous recombination deficient cancer cells. However, resistance to PARP inhibitors such as olaparib remains a problem in clinical use, and the mechanisms of resistance are not fully understood. To investigate mechanisms of PARP inhibitor resistance, we established a BRCA1 knockout clone derived from the pancreatic cancer MIA PaCa-2 cells, which we termed C1 cells, and subsequently isolated an olaparib-resistant C1/OLA cells. We then performed RNA-sequencing and pathway analysis on olaparib-treated C1 and C1/OLA cells. Our results revealed activation of cell signaling pathway related to NAD+ metabolism in the olaparib-resistant C1/OLA cells, with increased expression of genes encoding the NAD+ biosynthetic enzymes NAMPT and NMNAT2. Moreover, intracellular NAD+ levels were significantly higher in C1/OLA cells than in the non-olaparib-resistant C1 cells. Upregulation of intracellular NAD+ levels by the addition of nicotinamide also induced resistance to olaparib and talazoparib in C1 cells. Taken together, our findings suggest that upregulation of intracellular NAD+ is one of the factors underlying the acquisition of PARP inhibitor resistance.

Humans↗
PubMed2026

Targeted multiplex gene knockouts in Lemna minor using CRISPR/Cas9.

Lemna minor (commonly known as duckweed) is a fast-growing aquatic plant recognized as a promising green bioreactor for recombinant protein production. Its rapid proliferation, high protein yield, environmental adaptability, and edibility make it highly attractive for biotechnological applications. It is essential to develop and expand genetic tools tailored to this species to maximize these advantages and further unlock its biotechnological potential. A key strategy for achieving this goal is the implementation of advanced genome editing technologies, such as the CRISPR/Cas9 system. Although multiplex CRISPR/Cas9 gene editing has previously been successfully applied in Lemna aequinoctialis, the capability of the endogenous plant tRNA processing system for multiplex editing in L. minor using the polycistronic tRNA-sgRNA (PTG)/Cas9 system has not yet been explored. In this study, a PTG construct was engineered to include four sgRNAs designed to simultaneously target two plant-specific glycosyltransferase genes: α-1,3-fucosyltransferase (FucT) and β-1,2-xylosyltransferase (XylT). As anticipated, the PTG-Cas9 system successfully induced frameshift mutations, characterized by insertions and deletions (indels), in regenerated L. minor plants derived from transformed calli. Validation via PCR and RT-PCR analysis, followed by sequencing of the target loci, confirmed the presence of indels at the target sites. Furthermore, western blot analyses utilizing antibodies specific to XylT and FucT in two homozygous lines (lines 44 and 217) revealed truncated XylT proteins in both lines. Moreover, an in-frame FucT protein was detected in line 217, whereas FucT expression was absent in line 44. This study marked the first successful demonstration of PTG-Cas9 system for multiplex genome editing in L. minor, paving the way for advanced genetic engineering in this species.

CRISPR-Cas Systems↗
PubMed2026

CRISPR/Cas9-mediated knockout of PsLykX gene of pea (Pisum sativum L.) leads to loss of symbiotic nodules.

Pea (Pisum sativum L.) symbiosis with nodule bacteria supplying plants with additional nitrogen is a very specific plant-microbial interaction. Mutual recognition of the partners occurs through perception of bacterial signal molecules (Nod factors) by plant receptors, enabling bacterial entry via root hairs and formation of nitrogen-fixing nodules. The pea gene Sym2, described but not yet cloned, exists in different allelic forms defining the symbiotic specificity, and is therefore thought to encode a Nod factor receptor. The PsLykX gene is a strong candidate for the Sym2, since its alleles coincide with high or low symbiotic specificity; however, to date, no genetic evidence has been obtained for a role of PsLykX in symbiosis. Here, we knocked-out the PsLykX in European pea cultivar Caméor using Agrobacterium-mediated hairy root transformation and CRISPR-Cas9 editing. The roots with editing events confirmed by sequencing lost the ability to form nodules, providing direct functional evidence that PsLykX is essential, at least, for the symbiosis between pea cultivar Caméor and Rhizobium ruizarguesonis RCAM1026.

Pisum sativum↗
PubMed2024

Heterozygous knockout of Synaptotagmin13 phenocopies ALS features and TP53 activation in human motor neurons.

Spinal motor neurons (MNs) represent a highly vulnerable cellular population, which is affected in fatal neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). In this study, we show that the heterozygous loss of SYT13 is sufficient to trigger a neurodegenerative phenotype resembling those observed in ALS and SMA. SYT13+/- hiPSC-derived MNs displayed a progressive manifestation of typical neurodegenerative hallmarks such as loss of synaptic contacts and accumulation of aberrant aggregates. Moreover, analysis of the SYT13+/- transcriptome revealed a significant impairment in biological mechanisms involved in motoneuron specification and spinal cord differentiation. This transcriptional portrait also strikingly correlated with ALS signatures, displaying a significant convergence toward the expression of pro-apoptotic and pro-inflammatory genes, which are controlled by the transcription factor TP53. Our data show for the first time that the heterozygous loss of a single member of the synaptotagmin family, SYT13, is sufficient to trigger a series of abnormal alterations leading to MN sufferance, thus revealing novel insights into the selective vulnerability of this cell population.

Humans↗
PubMed2026

A novel triple-knockout allogeneic BCMA CAR T-cell therapy (CT0590) for multiple myeloma: preclinical and phase 1 study.

Host-versus-graft reaction (HVGR) is a major challenge in allogeneic chimeric antigen receptor (CAR) T-cell therapy. To counter host natural killer (NK) cell attacks, we armored allogeneic, HLA-I-deficient, B-cell maturation antigen (BCMA)-targeting CAR T cells with an NKG2A CAR. In vitro and animal studies demonstrated that allogeneic CAR-NKG2A T cells effectively resisted host NK cell-mediated killing. BCMA and NKG2A dual-targeting allogeneic CAR T cells (CT0590) resisted killing by NK cells and showed robust antitumor activity in preclinical in vivo models. On the basis of these data, a first-in-human study enrolled 5 patients (4 with relapsed and refractory multiple myeloma [RRMM] and 1 with primary plasma cell leukemia [pPCL]). CT0590 was well tolerated and caused no dose-limiting toxicities, treatment-related death, or graft-versus-host disease. Three patients achieved confirmed responses, including 2 with stringent complete response (sCR). Notably, sCR in the patient with RRMM was still ongoing (duration of response >23 months) at the time of data cutoff, and sCR in the patient with pPCL lasted for 20 months. Both patients showed robust expansion of universal CAR T cells (maximum concentration of >280 000 copies per μg genomic DNA) and higher baseline NKG2A expression on NK cells than nonresponders. These results suggest that CAR-NKG2A technology may overcome HVGR, especially in patients with elevated NKG2A expression on NK cells. Further studies of CT0590 in RRMM and pPCL are warranted. This trial was registered at www.clinicaltrials.gov as NCT05066022.

Humans↗
PubMed2026

Motor coordination and behavioural deficits in a mouse model of KMT2B-related dystonia.

INTRODUCTION: Pathogenic variants in KMT2B cause early-onset dystonia, but a mouse model that has undergone comprehensive, dystonia-oriented phenotyping is lacking. METHODS: We conducted detailed phenotyping on heterozygous Kmt2b constitutive knockout mice and wild-type littermates, assessing growth, neurobehavioural traits, motor coordination, sensorimotor gating, social behaviour and metabolic parameters, combined with striatal RNA sequencing. RESULTS: Kmt2b knockout mice of both sexes were viable but significantly smaller and lighter than littermate controls. Knockouts were hyperlocomotive in the open field and showed approximately two-fold larger acoustic startle responses; unexpectedly, prepulse inhibition was enhanced rather than reduced at all prepulse intensities. On the balance beam, knockouts crossed more slowly and paused more frequently; female knockouts also paused more on the ladder rung task. Frame-by-frame video analysis revealed a claw-like hindpaw posture characterized by abnormal inward flexion of the digits. Knockout mice spent less time investigating a novel conspecific, while social recognition memory remained intact. Striatal RNA sequencing confirmed reduction of Kmt2b transcript to approximately half of control levels and identified 177 differentially expressed genes, including Maob, encoding monoamine oxidase B; gene set enrichment analysis implicated neurodevelopmental, glial and mitochondrial processes. Nociception, vision, body-weight-adjusted grip strength, and clinical chemistry and haematological measures were largely unaffected. CONCLUSION: Heterozygous Kmt2b knockout mice show hyperlocomotion, altered sensorimotor gating, impaired motor coordination with dystonic-like paw posturing and reduced sociability, alongside a striatal transcriptomic signature implicating neurodevelopmental processes. The model mirrors aspects of human KMT2B-related dystonia and provides a platform for mechanistic study; environmental or pharmacological challenge may be needed to unmask overt dystonic features.

Dystonia↗
PubMed2026

Evaluation of germline transmission of electroporation-mediated double gene-edited cattle lines.

Gene editing in livestock using clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) offers a promising approach for genetic improvement in cattle. This study evaluated germline transmission and mutation stability of double-knockout cattle generated by zygote electroporation. Previously reported myostatin/beta-lactoglobulin (MSTN/BLG) and newly generated α-1,3-galactosyltransferase (GGTA1/BLG) double-knockout cattle were produced using CRISPR/Cas9-mediated genome editing. Targeted deep sequencing demonstrated extensive somatic mosaicism across multiple tissues. Computer-assisted sperm analysis (CASA) demonstrated normal sperm motility in MSTN/BLG double-knockout males. Fertilization of wild-type oocytes produced heterozygous embryos, with mutation frequencies of 37.76 ± 10.74% at the MSTN locus and 54.80 ± 7.73% at the BLG locus, as assessed by T7 endonuclease I (T7E1) assay. MSTN/BLG double-knockout sperm were subsequently used for embryo production and for artificial insemination of GGTA1/BLG double-knockout females. Healthy offspring were successfully obtained (n = 3), alongside one stillborn calf. Targeted deep sequencing of all four progenies revealed highly variable allele frequencies that deviated substantially from the approximately 50% expected for heterozygous germline transmission. In contrast, whole-genome sequencing (WGS) results were consistent with Mendelian expectations, underscoring the limitations of PCR-based targeted sequencing for assessing germline transmission in mosaic founders. These results show that CRISPR/Cas9-edited embryos generated by electroporation can develop into healthy, sexually mature cattle capable of germline transmission. While variable transmission rates were observed owing to founder mosaicism, non-mosaic F1 offspring were successfully generated. However, direct, embryo-mediated gene-editing strategies remain technically and economically challenging for large-scale commercial calf production, and reports in cattle are limited. This study provides a reference for future applications of gene-edited embryos and their germline propagation.

Animals↗
PubMed2025

The RNA-binding protein TRIM71 is essential for hearing in humans and mice and times auditory sensory organ development.

The RNA-binding protein TRIM71 is essential for brain development, and recent genetic studies in humans have identified TRIM71 as a risk gene for congenital hydrocephal-us (CH). Here, we show that monoallelic missense mutations in TRIM71 are associated with hearing loss (HL) and inner ear aplasia in humans. Utilizing conditional Trim71 knockout mice carrying a CH and HL-associated mutation, we demonstrate that loss of TRIM71 function during early otic development (embryonic day 9 to 10) causes severe HL. While inner ear morphogenesis occurs normally in Trim71 knockout mice, we find that early otic loss of TRIM71 function disrupts the highly stereotyped timing of cell cycle exit and differentiation within the inner ear auditory sensory organ (cochlea), resulting in the premature formation and innervation of mechanosensory hair cells. Transcriptomic profiling of Trim71-deficient cochlear progenitor cells identifies Inhba and Tgfbr2 as targets of TRIM71 repression, and our analysis of Inhba-Tgfbr1 double knockout mice indicates that TRIM71 maintains hair cell progenitors in a proliferative and undifferentiated state by restricting TGFβ-type signaling. Characterization of hair cells and their associated neurons in adult Trim71 knockout mice revealed reduced presynaptic terminals and neuronal degeneration in the outer hair cell region, providing a basis for the observed hearing deficits in Trim71 knockout mice.

Animals↗
PubMed2026

Phosphoproteomic Analysis of Cortical Tissue from Mice Lacking Both CaMKIIα and CaMKIIβ Identifies Novel In Vivo Substrates.

Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays a critical role in calcium signaling. Several studies have shown that mice with single Camk2a or Camk2b gene knockouts are viable, yet exhibit distinct phenotypes, whereas the double knockout of both genes is lethal. These findings indicate that each gene can have distinct roles and that they also partially compensate for each other in yet unknown essential brain functions. In order to provide insight into potential novel CaMKII functions, we performed parallel phosphoproteomic analyses on nonstimulated cortex tissues from inducible Camk2a and Camk2b double knockout (Camk2af/f;Camk2bf/f;CAG-CreESR) mice and from wild type mice. A total of 5622 phosphorylated peptides derived from 2080 proteins were identified. Phosphorylation at serine/threonine residues in 130 proteins was downregulated in the double knockout mice, including residues in 113 proteins that have not previously been identified as potential CaMKII substrates. Comparison of amino acid sequences surrounding the downregulated phosphorylation residues provided new insights into the CaMKII-substrate consensus sequences in vivo. This data set provides an important resource for future studies examining novel roles for CaMKII in the brain.

Animals↗