Ask about this productRelated genes to: CAMK2D Blocking Peptide
- Gene:
- CAMK2D NIH gene
- Name:
- calcium/calmodulin dependent protein kinase II delta
- Previous symbol:
- CAMKD
- Synonyms:
- -
- Chromosome:
- 4q26
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2016-04-06
Related products to: CAMK2D Blocking Peptide
Related articles to: CAMK2D Blocking Peptide
- Although heart disease arises from different etiologies, treatment remains largely one-size-fits-all, leaving many patients without optimal benefit, which highlights the need for cause-directed therapies. Pathogenic variants in RBM20, a cardiac splicing factor, lead to an aggressive form of dilated cardiomyopathy with high risk of ventricular arrhythmias. We hypothesized that the splicing target calcium/calmodulin-dependent kinase II delta (CAMK2D) is disease causing in RBM20 cardiomyopathy. Here we show that Rbm20/Camk2d double knockout mice are protected from heart failure and sudden cardiac death. In Rbm20-deficient hearts, phosphorylation of CAMK2D targets was increased, indicating that RBM20 loss results not only in mis-splicing of Camk2d transcripts but also in functional activation of CAMK2D signaling. Reexpression of individual CAMK2D splice variants in Rbm20/Camk2d double knockout mice reintroduced cardiac dysfunction, demonstrating that overactivation, rather than mis-splicing, drives disease. Treatment of Rbm20-p.Arg636Gln knockin mice with the ATP-competitive CAMK2 inhibitor hesperadin improved cardiac function. These findings identify CAMK2D overactivation as a central mechanism in RBM20 cardiomyopathy and support CAMK2D inhibition as a promising cause-directed therapy. - Source: PubMed
Publication date: 2026/05/04
van den Hoogenhof Maarten M GDuran JavierBritto-Borges ThiagoSequeira VascoKemmling ElenaKonrad LauraSchreiter FriederikeLennermann David CHartmann JoshuaSchraft LauraKornienko JuliaBock TheresaKrüger MarcusMaack ChristophDieterich ChristophSteinmetz Lars MDewenter MatthiasBacks Johannes - RBM20 (RNA binding motif protein 20) is a cardiac splicing factor responsible for the splicing of several cardiac genes such as titin (), triadin (), ryanodine receptor 2 (), PDZ and LIM domain protein 1 (), and calcium/calmodulin-dependent protein kinase II (). Pathogenic variants in are a major cause of familial dilated cardiomyopathy, and lead to missplicing of RBM20 target genes. - Source: PubMed
Publication date: 2026/04/30
Pant PriyankaHuang YongGhouse ZakiyaBai FangKemmling ElenaKonrad LauraAlameldeen AhmedKistler RebeccaSeeger TimonGotthardt MichaelParikh Victoria Nvan den Hoogenhof Maarten M G - Severe COVID-19 involves hyperinflammation and multiorgan pathology, but consistent gene signatures remain elusive. We aimed to identify consensus transcriptomic signatures and molecular mechanisms in severe COVID-19. We performed an integrative analysis of 39 studies spanning 11 tissue types, 1551 bulk RNA-seq samples, and over 2 million single cells. A vote-counting strategy combined with a systems-biology approach was applied to detect consensus differentially expressed genes (DEGs). Pathways related to interferon/TNF-α signaling, hypoxia response, and platelet activation were consistently enriched across data sets. Among consensus DEGs-such as IFITM3, BCL2A1, CAMK2D, and CCR1-RAB8B was prioritized for functional validation based on its recurrence in ~45% of tissues and its known role in vesicle trafficking, a process intimately linked to viral life cycles. Molecular dynamics simulations and in vitro assays in SARS-CoV-2-infected CaCo-2 cells demonstrated that RAB8B modulates VAMP-3 clustering and intracellular trafficking. Silencing of Rab8b-1 and Rab8b-2 reduced viral infection by 30% (p = 0.0302) and 76% (p < 0.001), respectively. This study defines robust consensus signatures and positions RAB8B as a critical host factor and potential therapeutic target in severe COVID-19. Further exploration of RAB8B inhibitors is warranted to explore therapeutic utility. An interactive database at https://covidatlas.sysbio.tools/. - Source: PubMed
Avila Jonathan PeñaPark PeterSingh YouvikaAmaral Paulo PCastro ÍcaroTen-Caten FelipeSchuch VivianeGonçalves André N AGiddaluru JeevanMorais Mauro César CafundóOgava Rodrigo L TLubiana Thiagode Castro Gabriel AmorosoAquino RodrigoDurão LuizMartins Júlia RaspanteJimenez LeandroCosta-Martins André GGonzalez-Dias PatríciaHirata Thiago Dominguez CrespoDias Thomaz LüscherPeixe Débora GuerraSimizo AdrianaE Silva Juan Carlo SantosVasconcelos Amanda PereiraRodrigues Marcelo BerçotCastelucci Bianca GVirgillio-da-Silva João VictorMenezes LarissaMoraes-Vieira Pedro MCabral-Marques OtavioNakaya Helder I - We have previously demonstrated that ovarian tumor (Otu) domain-containing ubiquitin aldehyde-binding protein 2 (Otub2), a deubiquitinating enzyme, exerts anti-apoptotic effects in primary human islets. The present study aims to further elucidate the molecular mechanisms underlying the role of Otub2 as a regulator of insulin secretion and β-cell function. - Source: PubMed
Oshry MichalIsaac RoiBoura-Halfon SigalitCasana EstefaniaSampson SanfordLev SimaBosch FatimaZick YehielVinik Yaron - The theory of visually guided ocular growth is well supported in explaining myopia, but how the retina senses focus versus defocus and converts the signaling into growth-modulating genetic signals remains unresolved. Using whole-cell recordings and single-cell RNA-seq in the mouse retina, we show that lateral inhibitory networks-horizontal cells in the outer retina, but not AII amacrine cells in the inner retina, respond to optical defocus. Dopaminergic amacrine cells (DACs) are maximally excited by focused images and increasingly inhibited by high blur, consistent with dopamine's anti-myopiagenic role. Single-cell RNA sequencing (scRNA-seq) revealed stable cell-class composition but coordinated, cell type-specific remodeling of gamma-aminobutyric acid (GABA)-ergic synapse and gap-junction pathways in lens-induced myopic (LIM) retinas. Consistent with a key role for retinal dopamine signaling, we found gene-level, cell-type-specific remodeling: and were significantly upregulated in highly myopic retinas, whereas multiple dopamine-pathway components (, , , , , , and ) were significantly downregulated. Together, our results support a general principle: neuromodulator-gated electrical coupling shapes computations for signal discrimination, and chronic sensory blur in LIM drives cross-level plasticity, from biophysical states to gene expression, that biases downstream coding and growth signals. Targeted manipulation of dopaminergic signaling may restore adaptive defocus encoding and slow myopic progression. Using lens-induced myopia as a model of blurred vision, we show that retinal circuits adapt to defocus in a cell type-specific way. Horizontal cell network, but not AII amacrine cell networks, alter their responses, whereas dopaminergic amacrine cells undergo early biophysical changes followed by transcriptional remodeling of the dopamine pathway. This cross-level adaptation, from synapses to gene expression, supports robust vision under uncertainty and suggests dopaminergic signaling as a target to restore healthy defocus encoding. - Source: PubMed
Publication date: 2026/03/30
So ChungHimZhang TingYang KangyiWang JiaJunYan-Yin Tse DennisPan Feng