Role Of Ca2 Research Articles

The calcium connection: exploring the intricacies of calcium signaling in plant-microbe interactions.

The process of plant immune response is orchestrated by intracellular signaling molecules. Since plants are devoid of a humoral system, they develop extensive mechanism of pathogen recognition, signal perception, and intricate cell signaling for their protection from biotic and abiotic stresses. The pathogenic attack induces calcium ion accumulation in the plant cells, resulting in calcium signatures that regulate the synthesis of proteins of defense system. These calcium signatures induct different calcium dependent proteins such as calmodulins (CaMs), calcineurin B-like proteins (CBLs), calcium-dependent protein kinases (CDPKs) and other signaling molecules to orchestrate the complex defense signaling. Using advanced biotechnological tools, the role of Ca2+ signaling during plant-microbe interactions and the role of CaM/CMLs and CDPKs in plant defense mechanism has been revealed to some extent. The Emerging perspectives on calcium signaling in plant-microbe interactions suggest that this complex interplay could be harnessed to improve plant resistance against pathogenic microbes. We present here an overview of current understanding in calcium signatures during plant-microbe interaction so as to imbibe a future direction of research.

Calcifuge and soil-indifferent Proteaceae from south-western Australia: novel strategies in a calcareous habitat

Background and aimsProteaceae are a prominent plant family in south-western Australia. Most Proteaceae are ‘calcifuge’, occurring exclusively on old phosphorus (P)-impoverished acidic soils, with a few ‘soil-indifferent’ species also found on young P-richer calcareous soils. Calcium (Ca)-enhanced P toxicity explains the calcifuge habit of Proteaceae. However, previous research has so far been focused exclusively on the roles of Ca and P in determining Proteaceae distribution, and consequently there is little knowledge on how other soil-based strategies influence this distribution. We aimed to study the effects of young calcareous soils on four soil-grown Proteaceae and assess differences between calcifuge and soil-indifferent Proteaceae to better understand their natural distribution.MethodsTwo calcifuge and two soil-indifferent Proteaceae from south-western Australia were grown in six contrasting soils, including young calcareous, and old acidic soils.ResultsWhen grown in calcareous soils all species showed root growth inhibition, micronutrient deficiency, Ca-enhanced P toxicity, and negative impacts on physiology. Calcifuge species were more sensitive to calcareous soils than soil-indifferent ones, although this varied between genera. Soil-indifferent species tended to produce more cluster roots, release more carboxylates per root mass, and allocate less Ca to their leaves, compared with calcifuges; they also had smaller seeds and were less sensitive to Ca-enhanced P toxicity.ConclusionWe surmise that a combination of these traits allows soil-indifferent species to tolerate calcareous soils. This study provides insight into how Proteaceae respond to young calcareous soils and how this influences their distribution.

Cell death induction and protection by activation of ubiquitously expressed anion/cation channels. Part 3: the roles and properties of TRPM2 and TRPM7.

Cell volume regulation (CVR) is a prerequisite for animal cells to survive and fulfill their functions. CVR dysfunction is essentially involved in the induction of cell death. In fact, sustained normotonic cell swelling and shrinkage are associated with necrosis and apoptosis, and thus called the necrotic volume increase (NVI) and the apoptotic volume decrease (AVD), respectively. Since a number of ubiquitously expressed ion channels are involved in the CVR processes, these volume-regulatory ion channels are also implicated in the NVI and AVD events. In Part 1 and Part 2 of this series of review articles, we described the roles of swelling-activated anion channels called VSOR or VRAC and acid-activated anion channels called ASOR or PAC in CVR and cell death processes. Here, Part 3 focuses on therein roles of Ca2+-permeable non-selective TRPM2 and TRPM7 cation channels activated by stress. First, we summarize their phenotypic properties and molecular structure. Second, we describe their roles in CVR. Since cell death induction is tightly coupled to dysfunction of CVR, third, we focus on their participation in the induction of or protection against cell death under oxidative, acidotoxic, excitotoxic, and ischemic conditions. In this regard, we pay attention to the sensitivity of TRPM2 and TRPM7 to a variety of stress as well as to their capability to physicall and functionally interact with other volume-related channels and membrane enzymes. Also, we summarize a large number of reports hitherto published in which TRPM2 and TRPM7 channels are shown to be involved in cell death associated with a variety of diseases or disorders, in some cases as double-edged swords. Lastly, we attempt to describe how TRPM2 and TRPM7 are organized in the ionic mechanisms leading to cell death induction and protection.

C-terminus of PIEZO1 governs Ca2+ influx and intracellular ERK1/2 signaling pathway in mechanotransduction

Cells sense and respond to extracellular mechanical stress through mechanotransduction receptors and ion channels, which regulate cellular behaviors such as cell proliferation and differentiation. Among them, PIEZO1, piezo-type mechanosensitive ion channel component 1, has recently been highlighted as a mechanosensitive ion channel in various cell types including mesenchymal stem cells. We previously reported that PIEZO1 is essential for ERK1/2 phosphorylation and osteoblast differentiation in bone marrow-derived mesenchymal stem cells (BMSCs), induced by hydrostatic pressure loading and treatment with the PIEZO1-specific activator Yoda1. However, the molecular mechanism underlying how PIEZO1 induces mechanotransduction remains unclear. In this study, we investigated that the role of the C-terminus in regulating extracellular Ca2+ influx and activating the ERK1/2 signaling pathway. We observed the activation of Fluo-4 AM in the Yoda1-stimulated human BMSC line UE7T-13, but not in a calcium-depleted cell culture medium. Similarly, Western blotting analysis revealed that Yoda1 treatment induced ERK1/2 phosphorylation, but this induction was not observed in calcium-depleted cell culture medium. To investigate the functional role of the C-terminus of PIEZO1, we generated HEK293 cells stably expressing the full-length mouse PIEZO1 (PIEZO1-FL) and a deletion-type PIEZO1 lacking the C-terminal intracellular region containing the R-Ras-binding domain (PIEZO1-ΔR-Ras). We found that Yoda1 treatment predominantly activated Flou-4 AM and ERK1/2 in PIEZO1-FL-trasfected cells but neither in PIEZO1-ΔR-Ras-transfected cells nor control cells. Our results indicate that the C-terminus of PIEZO1, which contains the R-Ras binding domain, plays an essential role in Ca2+ influx and activation of the ERK1/2 signaling pathway, suggesting that this domain is crucial for the mechanotransduction of osteoblastic differentiation in BMSCs.

Modulation and Regulation of Canonical Transient Receptor Potential 3 (TRPC3) Channels.

Canonical transient receptor potential 3 (TRPC3) channel is a non-selective cation permeable channel that plays an essential role in calcium signalling. TRPC3 is highly expressed in the brain and also found in endocrine tissues and smooth muscle cells. The channel is activated directly by binding of diacylglycerol downstream of G-protein coupled receptor activation. In addition, TRPC3 is regulated by endogenous factors including Ca2+ ions, other endogenous lipids, and interacting proteins. The molecular and structural mechanisms underlying activation and regulation of TRPC3 are incompletely understood. Recently, several high-resolution cryogenic electron microscopy structures of TRPC3 and the closely related channel TRPC6 have been resolved in different functional states and in the presence of modulators, coupled with mutagenesis studies and electrophysiological characterisation. Here, we review the recent literature which has advanced our understanding of the complex mechanisms underlying modulation of TRPC3 by both endogenous and exogenous factors. TRPC3 plays an important role in Ca2+ homeostasis and entry into cells throughout the body, and both pathological variants and downstream dysregulation of TRPC3 channels have been associated with a number of diseases. As such, TRPC3 may be a valuable therapeutic target, and understanding its regulatory mechanisms will aid future development of pharmacological modulators of the channel.

Reduced Cholecystokinin-Expressing Interneuron Input Contributes to Disinhibition of the Hippocampal CA2 Region in a Mouse Model of Temporal Lobe Epilepsy.

A significant proportion of temporal lobe epilepsy (TLE) patients experience drug-resistant seizures associated with mesial temporal sclerosis, in which there is extensive cell loss in the hippocampal CA1 and CA3 subfields, with a relative sparing of dentate gyrus granule cells and CA2 pyramidal neurons (PNs). A role for CA2 in seizure generation was suggested based on findings of a reduction in CA2 synaptic inhibition (Williamson and Spencer, 1994) and the presence of interictal-like spike activity in CA2 in resected hippocampal tissue from TLE patients (Wittner et al., 2009). We recently found that in the pilocarpine-induced status epilepticus (PILO-SE) mouse model of TLE there was an increase in CA2 intrinsic excitability associated with a loss of CA2 synaptic inhibition. Furthermore, chemogenetic silencing of CA2 significantly reduced seizure frequency, consistent with a role of CA2 in promoting seizure generation and/or propagation (Whitebirch et al., 2022). In the present study, we explored the cellular basis of this inhibitory deficit using immunohistochemical and electrophysiological approaches in PILO-SE male and female mice. We report a widespread decrease in the density of pro-cholecystokinin-immunopositive (CCK+) interneurons and a functional impairment of CCK+ interneuron-mediated inhibition of CA2 PNs. We also found a disruption in the perisomatic perineuronal net in the CA2 stratum pyramidale. Such pathologic alterations may contribute to an enhanced excitation of CA2 PNs and CA2-dependent seizure activity in the PILO-SE mouse model.SIGNIFICANCE STATEMENT Impaired synaptic inhibition in hippocampal circuits has been identified as a key feature that contributes to the emergence and propagation of seizure activity in human patients and animal models of temporal lobe epilepsy (TLE). Among the hippocampal subfields, the CA2 region is particularly resilient to seizure-associated neurodegeneration and has been suggested to play a key role in seizure activity in TLE. Here we report that perisomatic inhibition of CA2 pyramidal neurons mediated by cholecystokinin-expressing interneurons is selectively reduced in acute hippocampal slices from epileptic mice. Parvalbumin-expressing interneurons, in contrast, appear relatively conserved in epileptic mice. These findings advance our understanding of the cellular mechanisms underlying inhibitory disruption in hippocampal circuits in a mouse model of spontaneous recurring seizures.

New Insights into the Reparative Angiogenesis after Myocardial Infarction.

Myocardial infarction (MI) causes massive loss of cardiac myocytes and injury to the coronary microcirculation, overwhelming the limited capacity of cardiac regeneration. Cardiac repair after MI is finely organized by complex series of procedures involving a robust angiogenic response that begins in the peri-infarcted border area of the infarcted heart, concluding with fibroblast proliferation and scar formation. Efficient neovascularization after MI limits hypertrophied myocytes and scar extent by the reduction in collagen deposition and sustains the improvement in cardiac function. Compelling evidence from animal models and classical in vitro angiogenic approaches demonstrate that a plethora of well-orchestrated signaling pathways involving Notch, Wnt, PI3K, and the modulation of intracellular Ca2+ concentration through ion channels, regulate angiogenesis from existing endothelial cells (ECs) and endothelial progenitor cells (EPCs) in the infarcted heart. Moreover, cardiac repair after MI involves cell-to-cell communication by paracrine/autocrine signals, mainly through the delivery of extracellular vesicles hosting pro-angiogenic proteins and non-coding RNAs, as microRNAs (miRNAs). This review highlights some general insights into signaling pathways activated under MI, focusing on the role of Ca2+ influx, Notch activated pathway, and miRNAs in EC activation and angiogenesis after MI.

TRPM2: bridging calcium and ROS signaling pathways-implications for human diseases.

TRPM2 is a versatile and essential signaling molecule that plays diverse roles in Ca2+ homeostasis and oxidative stress signaling, with implications in various diseases. Research evidence has shown that TRPM2 is a promising therapeutic target. However, the decision of whether to activate or inhibit TRPM2 function depends on the context and specific disease. A deeper understanding of the molecular mechanisms governing TRPM2 activation and regulation could pave the way for the development of innovative therapeutics targeting TRPM2 to treat a broad range of diseases. In this review, we examine the structural and biophysical details of TRPM2, its involvement in neurological and cardiovascular diseases, and its role in inflammation and immune system function. In addition, we provide a comprehensive overview of the current knowledge of TRPM2 signaling pathways in cancer, including its functions in bioenergetics, oxidant defense, autophagy, and response to anticancer drugs.

Secretion of Interleukin 6 in Human Skeletal Muscle Cultures Depends on Ca2+ Signalling.

The systemic effects of physical activity are mediated by the release of IL-6 and other myokines from contracting muscle. Although the release of IL-6 from muscle has been extensively studied, the information on the cellular mechanisms is fragmentary and scarce, especially regarding the role of Ca2+ signals. The aim of this study was to characterize the role of the main components of Ca2+ signals in human skeletal muscle cells during IL-6 secretion stimulated by the Ca2+ mobilizing agonist ATP. Primary cultures were prepared from surgical samples, fluorescence microscopy was used to evaluate the Ca2+ signals and the stimulated release of IL-6 into the medium was determined using ELISA. Intracellular calcium chelator Bapta, low extracellular calcium and the Ca2+ channels blocker La3+ reduced the ATP-stimulated, but not the basal secretion. Secretion was inhibited by blockers of L-type (nifedipine, verapamil), T-type (NNC55-0396) and Orai1 (Synta66) Ca2+ channels and by silencing Orai1 expression. The same effect was achieved with inhibitors of ryanodine receptors (ryanodine, dantrolene) and IP3 receptors (xestospongin C, 2-APB, caffeine). Inhibitors of calmodulin (calmidazolium) and calcineurin (FK506) also decreased secretion. IL-6 transcription in response to ATP was not affected by Bapta or by the T channel blocker. Our results prove that ATP-stimulated IL-6 secretion is mediated at the post-transcriptional level by Ca2+ signals, including the mobilization of calcium stores, the activation of store-operated Ca2+ entry, and the subsequent activation of voltage-operated Ca2+ channels and calmodulin/calcineurin pathways.

The Role of Ca2+ Permeable AMPA Receptors in Neurodegeneration, Neurotoxicity, and Neuroinflammation.

It is believed that degenerative conditions that give rise to neurological diseases may share an abnormal influx of Ca2+, mainly through glutamate receptors. Current research on the glutamatergic system indicates that the N-methyl-D-aspartate receptor (NMDAR) is not the only receptor permeable to Ca2+. Under certain conditions, α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) are able to rapidly and potently mediate a neurotoxic Ca2+ influx. AMPARs are encoded by four genes designated GluR 1-4. The presence of the edited GluA2 subunit makes the heteromeric AMPAR impermeable to Ca2+ (CI-AMPAR's). On the other hand, the lack of GluA2 or disruptions in its post-translational editing result in Ca2+-permeable AMPA receptors (CP-AMPARs). In addition to triggering behavioral changes, the increase in CP-AMPARs is documented in several neurodegenerative, neuroinflammatory and neurotoxic conditions, demonstrating that AMPAR changes may play a role in the emergence and evolution of pathological conditions of the central nervous system (CNS). Seeking to better understand how CP-AMPARs influence CNS neuropathology, and how it may serve as a pharmacological target for future molecules, in this article, we summarize and discuss studies investigating changes in the composition of AMPARs and their cellular and molecular effects, to improve the understanding of the therapeutic potential of the CP-AMPAR in neurodegenerative, neurotoxic and neuroinflammatory diseases.

Calcium-doped magnetic humic acid nano particles for the efficient removal of heavy metals from wastewater: the role of Ca

ABSTRACT Ca doping is an effective method for improving the adsorption capacity of HA–Fe aggregates and regulating their structures. Understanding the structural characteristics of Ca–HA–Fe aggregates can help explore their microscopic adsorption effect on heavy metals. However, the heterogeneity of HA results in an incomplete understanding of the structural characteristics of the ternary system of Ca–HA–Fe aggregates and adsorption of the quaternary system of Ca–HA–Fe–Pb/Cu/Cd. In this study, interactions between Ca–HA–Fe ternary and Ca–HA–Fe–Pb/Cu/Cd quaternary systems were discussed from a molecular perspective. The structures of the basic structural units of HA were identified. Density functional theory (DFT) was employed to calculate the stable states of basic structural units of HA and Ca2+. The results showed that hydroxyl and carboxyl groups exhibited the highest capacity to bind with Ca2+. The interactions among Ca, HA, and Fe led to the formation of network aggregates. The binding energies of functional groups for heavy metals and the feasibility of ion exchange were calculated by the method of experiment and DFT. According to the contribution of functional group complexation and ion exchange, the ion exchange values for Pb2+, Cu2+, and Cd2+ were 66.71%, 62.87%, and 60.79%, respectively, which indicated that Ca2+ ion exchange showed considerable potential in enhancing the adsorption capacity of heavy metals.

EphrinB2 drives osteogenic fate of adult cardiac fibroblasts in a calcium influx dependent manner.

Cardiac calcification is a crucial but underrecognized pathological process, greatly increasing the risk of cardiovascular diseases. Little is known about how cardiac fibroblasts, as a central mediator, facilitate abnormal mineralization. Erythropoietin-producing hepatoma interactor B2 (EphrinB2), previously identified as an angiogenic regulator, is involved in fibroblast activation, while its role in the osteogenic differentiation of cardiac fibroblasts is unknown. Bioinformatics analysis was conducted to characterize the expression of the Ephrin family in human calcified aortic valves and calcific mouse hearts. The effects of EphrinB2 on cardiac fibroblasts to adopt osteogenic fate was determined by gain- and loss-of-function. EphrinB2 mRNA level was downregulated in calcified aortic valves and mouse hearts. Knockdown of EphrinB2 attenuated mineral deposits in adult cardiac fibroblasts, whereas overexpression of EphrinB2 promoted their osteogenic differentiation. RNA sequencing data implied that Ca2+-related S100/receptor for advanced glycation end products (RAGE) signaling may mediate EphrinB2-induced mineralization in cardiac fibroblasts. Moreover, L-type calcium channel blockers inhibited osteogenic differentiation of cardiac fibroblasts, implying a critical role in Ca2+ influx. In conclusion, our data illustrated an unrecognized role of EphrinB2, which functions as a novel osteogenic regulator in the heart through Ca2+ signaling and could be a potential therapeutic target in cardiovascular calcification.NEW & NOTEWORTHY In this study, we observed that adult cardiac fibroblasts but not neonatal cardiac fibroblasts exhibit the ability of osteogenic differentiation. EphrinB2 promoted osteogenic differentiation of cardiac fibroblasts through activating Ca2+-related S100/RAGE signaling. Inhibition of Ca2+ influx using L-type calcium channel blockers inhibited EphrinB2-mediated calcification of cardiac fibroblasts. Our data implied an unrecognized role of EphrinB2 in regulating cardiac calcification though Ca2+-related signaling, suggesting a potential therapeutic target of cardiovascular calcification.

TRPV3 Ion Channel: From Gene to Pharmacology.

Transient receptor potential vanilloid subtype 3 (TRPV3) is an ion channel with a sensory function that is most abundantly expressed in keratinocytes and peripheral neurons. TRPV3 plays a role in Ca2+ homeostasis due to non-selective ionic conductivity and participates in signaling pathways associated with itch, dermatitis, hair growth, and skin regeneration. TRPV3 is a marker of pathological dysfunctions, and its expression is increased in conditions of injury and inflammation. There are also pathogenic mutant forms of the channel associated with genetic diseases. TRPV3 is considered as a potential therapeutic target of pain and itch, but there is a rather limited range of natural and synthetic ligands for this channel, most of which do not have high affinity and selectivity. In this review, we discuss the progress in the understanding of the evolution, structure, and pharmacology of TRPV3 in the context of the channel's function in normal and pathological states.

Genome-Wide Identification and Expression Analysis of Calmodulin (CaM) and Calmodulin-Like (CML) Genes in the Brown Algae Saccharina japonica.

Calmodulins (CaMs) and Calmodulin-like proteins (CMLs) are vital in plant growth, development, and stress responses. However, CaMs and CMLs have not been fully identified and characterized in brown algae, which has been evolving independently of the well-studied green plant lineage. In this study, whole-genome searches revealed one SjCaM and eight SjCMLs in Saccharina japonica, and one EsCaM and eleven EsCMLs in Ectocarpus sp. SjCaM and EsCaM encoded identical protein products and shared 88.59-89.93% amino acid identities with Arabidopsis thaliana AtCaMs, thereby indicating that brown algae CaMs retained a similar Ca2+ sensors function as in plants. The phylogenetic and gene structure analysis results showed that there was significant divergence in the gene sequences among brown algae CMLs. Furthermore, evolutionary analysis indicated that the function of brown alga CMLs was relatively conserved, which may be related to the fact that brown algae do not need to face complex environments like terrestrial plants. Regulatory elements prediction and the expression analysis revealed the probable functioning of SjCaM/CML genes in gametophyte development and the stress response in S. japonica. In addition, the SjCaM/SjCMLs interacting proteins and chemicals were preliminarily predicted, suggesting that SjCaM/SjCMLs might play putative roles in Ca2+/CaM-mediated growth and development processes and stimulus responses. Therefore, these results will facilitate our understanding of the evolution of brown algae CaMs/CMLs and the functional identification of SjCaM/SjCMLs.

The role of Ca on the microstructure and tensile properties of Mg-Al-Zn-Ca alloys

Synergy between Ca and other alloying elements such as Al and Zn can modify the microstructure and mechanical properties of Mg alloys. In this work, we compared four extrusion alloys: Mg-6Al-2 Zn, Mg-6Al-2Zn-0.5Ca, Mg-6Al-2Zn-1.0Ca, and Mg-6Al-2Zn-2.0Ca (all in wt.%). Tensile properties were remarkably not improved with Ca addition. The underlying reasons were explored using in situ synchrotron X-ray diffraction, electron microscopy, and cyclic loading tests. It is found that solute Ca imposes a softening effect on Mg's slip systems. The slight increase of the yield strength by the formation of Al2Ca particles is fully offset by the reduced Al solute strengthening. Texture weakening and resultant ductility enhancement reported in Mg-Zn-Ca ternary alloys is largely compromised by the high amount of Al. Nevertheless, Al2Ca particles can enhance the materials’ strain hardening by inducing back stress. An elastic-viscoplastic self-consistent (EVPSC) model was employed to simulate the deformation of the four alloys. Discrepancies between the simulation results and the experimental measurements mostly occur in the microscopic level (e.g. lattice strains and dislocation density evolution), and the reasons will be discussed.

Comparing confocal and two-photon Ca2+ imaging of thin low-scattering preparations

Ca2+ imaging provides insight into biological processes ranging from subcellular dynamics to neural network activity. Two-photon microscopy has assumed a dominant role in Ca2+ imaging. The longer wavelength infra-red illumination undergoes less scattering, and absorption is confined to the focal plane. Two-photon imaging can thus penetrate thick tissue ∼10-fold more deeply than single-photon visible imaging to make two-photon microscopy an exceptionally powerful method for probing function in intact brain. However, two-photon excitation produces photobleaching and photodamage that increase very steeply with light intensity, limiting how strongly one can illuminate. In thin samples, illumination intensity can assume a dominant role in determining signal quality, raising the possibility that single-photon microscopy may be preferable. We therefore tested laser scanning single-photon and two-photon microscopy side by side with Ca2+ imaging in neuronal compartments at the surface of a brain slice. We optimized illumination intensity for each light source to obtain the brightest signal without photobleaching. Intracellular Ca2+ rises elicited by one action potential had twice the signal/noise ratio with confocal as with two-photon imaging in axons, were 31% higher in dendrites, and about the same in cell bodies. The superior performance of confocal imaging in finer neuronal processes likely reflects the dominance of shot noise when fluorescence is dim. Thus, when out-of-focus absorption and scattering are not issues, single-photon confocal imaging can yield better quality signals than two-photon microscopy.

Role of CA 19.9 and CEA in predicting diagnosis in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is responsible for 90% of cases of primary liver cancer and is also responsible for the fourth most common cause of cancer death worldwide. To improve the current scenario for the early diagnosis and management of HCC patients, a better understanding of HCC is required. Hence, serum tumor biomarkers such as CA 19-9 (cancer antigen), CEA (carcinoembryonic antigen), and AFP (alpha-fetoprotein) show promising future, when it comes to early diagnosis of primary liver cancer (PHC), liver cirrhosis, and metastasis. It was a retrospective cross-sectional analysis of patients diagnosed with primary hepatocellular carcinoma, data were collected from the hospital database and included a total of 245 patients of HCC attending the out-patient department and some were admitted for treatment at our institution. Out of 245 patients, 68 patients were selected for the study. We have collected information related to the patient's demographic profile, pathological diagnosis, biochemical profile, and even radiological diagnosis. The sensitivity and specificity of CA 19-9 and CEA were also done. Adenocarcinoma is the most common type of liver cancer followed by HCC. We have shown a weak correlation between tumor markers CA 19-9 and CEA for the diagnosis of liver carcinoma. Further our study shows that the sensitivity of tumor marker CA 19-9 for the diagnosis of liver carcinoma is 64.28% and that of CEA is 83.67%. The search for a novel biomarker of early liver carcinoma requires further research. The authors declare that they have no competing interests.

Role of Ca2+ doping on the structure, magnetic, and magnetocaloric properties of La0.75Gd0.05Sr0.2−xCaxMnO3 (x = 0, 0.05, 0.075, and 0.10) perovskite manganites

Role of Ca2+ doping on the structure, magnetic, and magnetocaloric properties of La0.75Gd0.05Sr0.2−xCaxMnO3 (x = 0, 0.05, 0.075, and 0.10) perovskite manganites

Regulation of Cardiac Cav1.2 Channels by Calmodulin

Cav1.2 Ca2+ channels, a type of voltage-gated L-type Ca2+ channel, are ubiquitously expressed, and the predominant Ca2+ channel type, in working cardiac myocytes. Cav1.2 channels are regulated by the direct interactions with calmodulin (CaM), a Ca2+-binding protein that causes Ca2+-dependent facilitation (CDF) and inactivation (CDI). Ca2+-free CaM (apoCaM) also contributes to the regulation of Cav1.2 channels. Furthermore, CaM indirectly affects channel activity by activating CaM-dependent enzymes, such as CaM-dependent protein kinase II and calcineurin (a CaM-dependent protein phosphatase). In this article, we review the recent progress in identifying the role of apoCaM in the channel 'rundown' phenomena and related repriming of channels, and CDF, as well as the role of Ca2+/CaM in CDI. In addition, the role of CaM in channel clustering is reviewed.

Calcium signalling in weeds under herbicide stress: An outlook.

The continuous use of herbicides for controlling weeds has led to the evolution of resistance to all major herbicidal modes of action globally. Every year, new cases of herbicide resistance are reported. Resistance is still in progress in many species, which must be stopped before it becomes a worldwide concern. Several herbicides are known to cause stressful conditions that resemble plant abiotic stresses. Variation in intracellular calcium (Ca2+) concentration is a primary event in a wide range of biological processes in plants, including adaptation to various biotic and abiotic stresses. Ca2+ acts as a secondary messenger, connecting various environmental stimuli to different biological processes, especially during stress rejoindering in plants. Even though many studies involving Ca2+ signalling in plants have been published, there have been no studies on the roles of Ca2+ signalling in herbicide stress response. Hence, this mini-review will highlight the possible sensing and molecular communication via Ca2+ signals in weeds under herbicide stress. It will also discuss some critical points regarding integrating the sensing mechanisms of multiple stress conditions and subsequent molecular communication. These signalling responses must be addressed in the future, enabling researchers to discover new herbicidal targets.