What is calmodulin protein

The disease is caused by variants affecting the gene represented in this entry. Disease description An arrhythmogenic disorder characterized by stress-induced, bidirectional ventricular tachycardia that may degenerate into cardiac arrest and cause sudden death.

Patients present with recurrent syncope, seizures, or sudden death after physical activity or emotional stress. CPVT4 inheritance is autosomal dominant. FEBS Lett. Disease description A form of long QT syndrome, a heart disorder characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress, and can present with a sentinel event of sudden cardiac death in infancy.

Proteomics M Bienvenut W. Proteome Res. Ubiquitination results in a strongly decreased activity. By similarity. Phosphorylation results in a decreased activity.

Interacts with MYO10 By similarity. Interacts with SYT7 By similarity. Protein Pept. Cell Biol. Cell Rep. EMBO J. Belongs to the calmodulin family. The information is filed in different subsections. Length: Mass Da : 16, It is useful for tracking sequence updates. The algorithm is described in the ISO standard. Calmodulin 3 Phosphorylase kinase, Full view. These are stable identifiers and should be used to cite UniProtKB entries. Upon integration into UniProtKB, each entry is assigned a unique accession number, which is called 'Primary citable accession number'.

Do not show this banner again. One common calcium-binding motif is the EF-hand, but other calcium-binding motifs also exist. Calcium , Metal-binding. Pathway Commons web resource for biological pathway data More PathwayCommons i. Reactome - a knowledgebase of biological pathways and processes More Reactome i. MoonDB Database of extreme multifunctional and moonlighting proteins More MoonDB i. Homo sapiens Human. This is known as the 'taxonomic identifier' or 'taxid'.

It lists the nodes as they appear top-down in the taxonomic tree, with the more general grouping listed first. Vadassery, J. CMLmediated calcium signaling coordinates responses to Spodoptera herbivory and abiotic stresses in Arabidopsis.

Scholz, S. Mutation of the Arabidopsis calmodulin-like protein CML37 deregulates the jasmonate pathway and enhances susceptibility to herbivory. Plant 7 , — Rick, C. Genetic variation in Solanum pennellii: comparisons with two other sympatric tomato species. Plant Syst. Lespinet, O. The role of lineage-specific gene family expansion in the evolution of eukaryotes.

Genome Res 12 7 , — Konstantinidis, K. Trends between gene content and genome size in prokaryotic species with larger genomes. Fischer, I. Impact of recurrent gene duplication on adaptation of plant genomes.

BMC Plant Biol 14 , Guo, Y. Gene family evolution in green plants with emphasis on the origination and evolution of Arabidopsis thaliana genes. A rice membrane-bound calcium-dependent protein kinase is activated in response to low temperature. Roy, S. The evolution of spliceosomal introns: patterns, puzzles and progress.

Day, I. Analysis of EF-hand-containing proteins in. Genome Biol. Xu, W. Characterization of a novel stilbene synthase promoter involved in pathogen- and stress-inducible expression from Chinese wild Vitis pseudoreticulata. Planta 2 , — Delk, N. Magnan, F. Mutations in AtCML9, a calmodulin-like protein from arabidopsis thaliana, alter plant responses to abiotic stress and abscisic acid. Plant J 56 , — Vanderbeld, B. Yin, X. OsCML4 improves drought tolerance through scavenging of reactive oxygen species in rice.

Plant Biol. Yu, H. Differential regulation of calmodulin, phenylalanine ammonia-lyase, and salicylic acid in response to Botrytis cinerea infection in tomato with different Ca2C concentrations. Journal of Plant Nutrition 41 6 , 1—15 ADS Google Scholar.

Hu, D. Plant , — Download references. This work was supported by grants from the Beijing innovation team construction project The funders had no role in study design, data collection, data analysis, decision to publish, or preparation of the manuscript.

You can also search for this author in PubMed Google Scholar. Conceived and designed the experiments: J. Performed the experiments: J. Analyzed the data: J. Wrote the paper: J. Provided guidance on the whole study: J. S and X. Correspondence to Xiangge Du. Reprints and Permissions. Shi, J. Identification, characterization and expression analysis of calmodulin and calmodulin-like proteins in Solanum pennellii.

Sci Rep 10, Download citation. Received : 22 September Accepted : 26 February Published : 04 May Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Plant Molecular Biology Plant Physiology Reports By submitting a comment you agree to abide by our Terms and Community Guidelines.

If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Advanced search. Skip to main content Thank you for visiting nature. Download PDF. Subjects Plant physiology Plant stress responses. Abstract In plants, the calmodulin CaM proteins is an important calcium-binding protein, which play a crucial role in both regulating plant growth and development, as well as in the resistance mechanisms to various biotic and abiotic stresses.

Introduction Plants are invariably subjected to stressful environmental conditions and pathogenic attacks from various bacteria, fungi, and viruses throughout their lives. Full size table. Figure 1. Full size image. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7.

Table 5 The number of genes on the chromosomes of Solanum pennellii. Plant materials In this study, wild cultivar Solanum pennellii LA was used. It is known that elements, such as the immune system, can mediate the communication between them. In an inflammatory process as observed during CKD and chronic heart failure CHF , cytokines are released by circulating and tissue-resident inflammatory cells monocytes mainly and play an important role in the progression of these diseases Yogasundaram et al.

In CRS, the tissue injury is strongly followed by inflammation. Many inflammatory cytokines are enhanced in experimental models of renal ischemia TNF-a, IL-1, and IL-6 and also markers, including the factor nuclear kappa B NF-kB , which is very important for cell signaling during inflammatory processes Trentin-Sonoda et al. During cardiac ischemia, myocytes release inflammatory cytokines Colombo et al. Colombo et al. Inflammation also causes progressive renal dysfunction and fibrosis, which continues to injure the organ, maintaining the cycle.

Additionally, inflammation leads to the release of renin, activating the renin-angiotensin-aldosterone system RAAS , which activates the sympathetic nervous system SNS by increasing serum norepinephrine concentrations and is the cause of ROS release from the inflammatory cells Bongartz et al. As mentioned above and summarized by Rusciano et al. There are many blockers and inhibitors used nowadays in research.

The first inhibitor described was KN in Tokumitsu et al. One year later, in , Sumi M and collaborators described a new and more selective inhibitor called KN Sumi et al. It was already discovered that KN can directly block the potassium current I Kr and potassium voltaged channels, preventing arrhythmic properties of CamKII Mustroph et al. Some studies have proven the efficiency of KN in heart pathologies in several animal models. Under in vitro and in vivo stimulations with isoproterenol, arrhythmias have been abolished after using NK Sag et al.

On some models, the KN does not seem to prevent but to slow the arrhythmia as longer cycle length without marked alterations in baseline ECG characteristics Hoeker et al.

Another study shows the high capacity to inhibit the binding of CaM with Na V 1. Experiments using TG RYR-mutant mice SD mutant are naturally more susceptible to atrial fibrillation, and because of this, it is used as a well-established model.

It is the most used one in studies that require the blocking of CaMKII, and it is resistant even to proteolysis. As mentioned, AC3-I is derived from autocamtide As the research regarding CaMKII increases, its therapeutic use implicated in pharmaceuticals has been studied more.

Several studies, using these inhibitors mentioned above, impart a cardio protection. This is the main reason it is used more in the studies concerning the participation of CaMKII in many cell functions. Studies using this blocker also imply cardio protection: preventing hypertrophy, reducing ventricular arrhythmias, improving mechanical function, reducing RyR2 lacking, and decreasing mortality of diabetic mice Sag et al.

Some studies have proven the efficiency of AC3-I in pathologies in some animal models. CRS, already cited, seems to be one of them.

Both kidneys and heart share many mechanisms of homeostasis, and any injury to one can lead to one in the other. The close relation between inflammation and oxidative stress in pathophysiological processes also makes the balance between oxidant and antioxidant forces and, therefore, oxidative stress, one of the most important mechanisms as has been demonstrated in heart and kidney injury studies Li et al. Some of these pathologies include left ventricle hypertrophy, atherosclerosis, endothelial dysfunction, and fibrosis in the heart while in the kidney ROS promotes interstitial fibrosis and increased inflammation Kumar et al.

Oxidative stress triggers an inflammatory response, and this response induces more oxidative stress. This stress may be maintaining the previously mentioned cycle of damage. Erickson et al. Some proteins maintain a redox sensor that regulates the cell response to oxidative stress Kim et al.

CaM is one of these proteins, and this oxidation leads to a regulatory cascade response with specific targets, including CaMKII Snijder et al. This isoform of NOS produces an excessive amount of NO that mediates impaired vasoconstriction, which may be further worsened by the decreased of eNOS activity Jian et al.

In addition, studies have shown the role of NOS in the kidney, demonstrating that, when NOS activity is compromised, there are a series of renal dysfunctions that reduce glomerular perfusion and filtration, which may lead to a progressive scenario of hypertension and kidney injuries Carlstrom and Montenegro, On the other hand, Kong et al. In addition to the redox balance, other factors indirectly contribute to cardiac and renal alterations.

Many approaches have been studied in order to set a start point for the CRS. One of them is epigenetics factors. Epigenetics is the area of biology that studies changes in the functioning of a gene that is not caused by alterations in the DNA sequence and that perpetuate in the meiotic or mitotic cell divisions Wu and Morris, Epigenetic modifications are highly coordinated processes of change that are not restricted to a specific phase of life. These characteristics are fundamental to diseases acquired throughout life.

Studies have been developed to innovate the way to prevent CRS. Slowly, epigenetics is gaining space, and traditional mechanisms such as RAAS and inflammation are being replaced by other patterns of findings and prevention. Imaging the scale of modifications and mutations in a syndrome such as CRS, numerous cell lines may be altered and reprogrammed, in both heart and kidney. Studies have pointed out the role of epigenetics in the development of CRS Gaikwad et al.

In types 3 and 4, for example, renal failure increases cardiac histone H3 epigenetics, evidencing the crosstalk between renal failure and the transcription of cardiomyopathy-related genes Gaikwad et al. It is important to mention that epigenetics in CRS itself are little studied when compared to the traditional mechanisms even though it is very promising.

The focus of studies is linked to inflammation and oxidative stress, which we know to be the consequences of CRS. During HF independent of renal injury, we can note the expression of transcription factors, angiogenic factors, and natriuretic factors, often used as biomarkers of this condition.

Epigenetic modifications regulate them. Pathological hypertrophy and compromised contractility are described to increase DNA methylation levels. This connection can lead to CRS types 1 and 2 and can be strongly linked to the diagnosis of heart dysfunction. In addition, it is extremely important to highlight the role of micro RNA miR. To identify signaling pathways, there is a serviceable tool called gene set analysis GSA. It uses statistical analysis to predefine gene sets involved in a specific cellular process.

For example, miR has a key role during cardiac hypertrophy. Given that, miR is also a potent therapeutic target for cardiac diseases Brown et al. In addition, Kim et al. It is worth mentioning the role of miR-1, once alterations in its expression or inhibition have been discovered in many cardiac pathologies Yang et al.

Recently, Zhang et al. Regarding inflammatory processes, miRp has been illustrated to inhibit inflammatory response in human bronchial epithelial cells and is downregulated in heart diseases once miRp is able to inhibit STAT3 and reduce the expression of CaMKII. In relation to kidney disease, Park et al.

In addition, recent studies have focused on MiR regulation and exosomes, specialized nanosized membranous vesicles, in different experimental models. These membrane-bound vesicles 30— nm are released from different cell types and deliver bioactive molecules, including microRNAs miRs.

Previous studies report that lncRNAs play critical roles in the modulation of heart development and cardiovascular diseases Wang et al. For example, Shao et al. The evidence in the literature suggests that CaMKII is a key molecule for understanding the physiology and physiopathology of cardiovascular diseases as well as a prominent target for new strategies of treatment.

Figure 2. CJ and MC-R proposed the idea and writing. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Alarcon, M. Alfazema, N. Camk2n1 is a negative regulator of blood pressure, left ventricular mass, insulin sensitivity, and promotes adiposity.

Hypertension 74, — Anavekar, N. Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction. Anbanandam, A. Mediating molecular recognition by methionine oxidation: conformational switching by oxidation of methionine in the carboxyl-terminal domain of calmodulin.

Biochemistry 44, — PDB helps teachers, students, and the general public explore the 3D world of proteins and nucleic acids. Learning about their diverse shapes and functions helps to understand all aspects of biomedicine and agriculture, from protein synthesis to health and disease to biological energy.

Why PDB? PDB builds introductory materials to help beginners get started in the subject "", as in an entry level course as well as resources for extended learning. Toggle navigation PDB Educational portal of. Molecule of the Month. Calmodulin Calcium ions rapidly deliver signals to control processes such as muscle contraction, nerve signaling, and fertilization Calmodulin, with bound calcium in turquoise.

Calcium is the most plentiful mineral element found in your body, with phosphorous coming in second. This probably doesn't come as a surprise, since your bones are strengthened and supported by about two kilograms of calcium and phosphorous. Your body also uses a small amount of calcium, in the form of calcium ions, to perform more active duties.

Calcium ions play essential roles in cell signaling, helping to control processes such as muscle contraction, nerve signaling, fertilization and cell division.

Through the action of calcium pumps and several kinds of calcium binding proteins, cells keep their internal calcium levels , times lower than the calcium levels in the blood. Thus when calcium is released into cells, it can interact with calcium sensing proteins and trigger different biological effects, causing a muscle to contract, releasing insulin from the pancreas, or blocking the entry of additional sperm cells once an egg has been fertilized.