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1.
Konstantin N. Belosludtsev Nils-Erik L. Saris Natalia V. Belosludtseva Alexander S. Trudovishnikov Lyudmila D. Lukyanova Galina D. Mironova 《Journal of bioenergetics and biomembranes》2009,41(4):395-401
Earlier we found that being added to rat liver mitochondria, palmitic acid (Pal) plus Ca2+ opened a cyclosporin A-insensitive pore, which remained open for a short time. Apparently, this pore is involved in the Pal-induced
apoptosis and may also take part in the mitochondrial Ca2+ recycling as a Ca2+ efflux system (Belosludtsev et al. J Bioenerg Biomembr 38:113–120, 2006; Mironova et al. J. Bioenerg. Biomembr. 39:167–174, 2007). In this paper, we continue studying physiological and regulatory aspects of the pore. The following observations have been
made. (1) Cardiolipin has been found to facilitate the Ca2+-induced formation of pores in the Pal-containing liposomal membranes. (2) The opening of Pal/Ca2+-induced pore is accompanied by the release of apoptosis-induced factor (AIF) from mitochondria. (3) The rate of Pal/Ca2+-induced swelling of rat liver mitochondria increases substantially with the age of animals. (4) Although the Pal/Ca2+-induced pore opens both in the liver and heart mitochondria, the latter require higher Pal concentrations for the pore to
open. (5) The pore opening depends on the resistance of animals to hypoxia: in the highly resistant to hypoxia rats, the mitochondrial
Pal/Ca2+-induced pore opens easier than in the low resistant animals, this being opposite for the classical, cyclosporin A-sensitive
MPT pore. The adaptation of the low resistant rats to oxygen deficiency increases the sensitivity of their mitochondria to
PalCaP inductors. The paper also discusses a possible role of the mitochondrial Pal/Ca2+-induced pore in the protection of tissues against hypoxia. 相似文献
2.
The photosystem II (PSII) manganese-stabilizing protein (PsbO) is known to be the essential PSII extrinsic subunit for stabilization
and retention of the Mn and Cl− cofactors in the oxygen evolving complex (OEC) of PSII, but its function relative to Ca2+ is less clear. To obtain a better insight into the relationship, if any, between PsbO and Ca2+ binding in the OEC, samples with altered PsbO-PSII binding properties were probed for their potential to promote the ability
of Ca2+ to protect the Mn cluster against dark-inhibition by an exogenous artificial reductant, N,N-dimethylhydroxylamine. In the absence of the PsbP and PsbQ extrinsic subunits, Ca2+ and its surrogates (Sr2+, Cd2+) shield Mn atoms from inhibitory reduction (Kuntzleman et al., Phys Chem Chem Phys 6:4897, 2004). The results presented here show that PsbO exhibits a positive effect on Ca2+ binding in the OEC by facilitating the ability of the metal to prevent inhibition of activity by the reductant. The data
presented here suggest that PsbO may have a role in the formation of the OEC-associated Ca2+ binding site by promoting the equilibrium between bound and free Ca2+ that favors the bound metal. 相似文献
3.
Zachary Cooper Michael Greenwood Borbala Mazzag 《Bulletin of mathematical biology》2009,71(7):1543-1579
We investigate the role of heterogeneous expression of IP3R and RyR in generating diverse elementary Ca2+ signals. It has been shown empirically (Wojcikiewicz and Luo in Mol. Pharmacol. 53(4):656–662, 1998; Newton et al. in J. Biol. Chem. 269(46):28613–28619, 1994; Smedt et al. in Biochem. J. 322(Pt. 2):575–583, 1997) that tissues express various proportions of IP3 and RyR isoforms and this expression is dynamically regulated (Parrington et al. in Dev. Biol. 203(2):451–461, 1998; Fissore et al. in Biol. Reprod. 60(1):49–57, 1999; Tovey et al. in J. Cell Sci. 114(Pt. 22):3979–3989, 2001). Although many previous theoretical studies have investigated the dynamics of localized calcium release sites (Swillens
et al. in Proc. Natl. Acad. Sci. U.S.A. 96(24):13750–13755, 1999; Shuai and Jung in Proc. Natl. Acad. Sci. U.S.A. 100(2):506–510, 2003a; Shuai and Jung in Phys. Rev. E, Stat. Nonlinear Soft Matter Phys. 67(3 Pt. 1):031905, 2003b; Thul and Falcke in Biophys. J. 86(5):2660–2673, 2004; DeRemigio and Smith in Cell Calcium 38(2):73–86, 2005; Nguyen et al. in Bull. Math. Biol. 67(3):393–432, 2005), so far all such studies focused on release sites consisting of identical channel types. We have extended an existing mathematical
model (Nguyen et al. in Bull. Math. Biol. 67(3):393–432, 2005) to release sites with two (or more) receptor types, each with its distinct channel kinetics. Mathematically, the release
site is represented by a transition probability matrix for a collection of nonidentical stochastically gating channels coupled
through a shared Ca2+ domain. We demonstrate that under certain conditions a previously defined mean-field approximation of the coupling strength
does not accurately reproduce the release site dynamics. We develop a novel approximation and establish that its performance
in these instances is superior. We use this mathematical framework to study the effect of heterogeneity in the Ca2+-regulation of two colocalized channel types on the release site dynamics. We consider release sites consisting of channels
with both Ca2+-activation and inactivation (“four-state channels”) and channels with Ca2+-activation only (“two-state channels”) and show that for the appropriate parameter values, synchronous channel openings within
a release site with any proportion of two-state to four-state channels are possible, however, the larger the proportion of
two-state channels, the more sensitive the dynamics are to the exact spatial positioning of the channels and the distance
between channels. Specifically, the clustering of even a small number of two-state channels interferes with puff/spark termination
and increases puff durations or leads to a tonic response. 相似文献
4.
Ho SW Jung D Calhoun JR Lear JD Okon M Scott WR Hancock RE Straus SK 《European biophysics journal : EBJ》2008,37(4):421-433
Daptomycin, a cyclic anionic lipopeptide antibiotic, whose three-dimensional structure was recently solved using solution
state NMR (Ball et al. 2004; Jung et al. 2004; Rotondi and Gierasch 2005), requires calcium for function. To date, the exact nature of the interaction between divalent cations, such as Ca2+ or Mg2+, has not been fully characterized. It has, however, been suggested that addition of Ca2+ to daptomycin in a 1:1 molar ratio induces aggregation. Moreover, it has been suggested that certain residues, e.g. Asp3
and Asp7, which are essential for activity (Grunewald et al. 2004; Kopp et al. 2006), may also be important for Ca2+ binding (Jung et al. 2004). In this work, we have tried: (1) to further pinpoint how Ca2+ affects daptomycin structure/oligomerization using analytical ultracentrifugation; and (2) to determine whether a specific
calcium binding site exists, based on one-dimensional 13C NMR spectra and molecular dynamics (MD) simulations. The centrifugation results indicated that daptomycin formed micelles
of between 14 and 16 monomers in the presence of a 1:1 molar ratio of Ca2+ and daptomycin. The 13C NMR data indicated that addition of calcium had a significant effect on the Trp1 and Kyn13 residues, indicating that either
calcium binds in this region or that these residues may be important for oligomerization. Finally, the molecular dynamics
simulation results indicated that the conformational change of daptomycin upon calcium binding might not be as significant
as originally proposed. Similar studies on the divalent cation Mg2+ are also presented. The implication of these results for the biological function of daptomycin is discussed.
Electronic supplementary material The online version of this article (doi:) contains Supplemental Material, which is available to authorized users.
Steven W. Ho and David Jung have contributed equally to this work. 相似文献
5.
A significant amount of Ca2+ is contained in secretory mucin granules. Exchange of Ca2+ for monovalent cations drives the process of mucin decondensation and hydration after fusion of granules with the plasma
membrane. Here we report direct observation of calcium secretion with a Ca2+ ion-selective electrode (ISE) in response to apical stimulation with ATP from HT29-Cl.16E cells, a subclone of the human
colonic cancer cell line HT29. No increase in Ca2+ level was seen for the sister cell line Cl.19A, which lacks mucin granules, or for Cl.16E cells after inhibition of granule
fusion with wortmannin. Further, the measured concentration was used to estimate the time-resolved rate of release of Ca2+ from the cell monolayer, by use of a deconvolution-based method developed previously (Nair and Gratzl in Anal Chem 77:2875–2881,
2005). The results argue that Ca2+ release by Cl.16E cells is associated specifically with mucin secretion, i.e., that the measured Ca2+ increase in the apical solution is derived from granules after fusion and mucin exocytosis. The Ca2+ ISE in conjunction with deconvolution provides a minimally disturbing method for assessment of Ca2+ secretion rates. The release rates provide estimates of exocytosis rates and, when combined with earlier capacitance measurements,
estimates of post-stimulation endocytosis rates also. 相似文献
6.
Mariya V. Kovaleva Evgeniya I. Sukhanova Tatyana A. Trendeleva Marina V. Zyl’kova Ludmila A. Ural’skaya Kristina M. Popova Nils-Erik L. Saris Renata A. Zvyagilskaya 《Journal of bioenergetics and biomembranes》2009,41(3):239-249
In this study we used tightly-coupled mitochondria from Yarrowia lipolytica and Dipodascus (Endomyces) magnusii yeasts, possessing a respiratory chain with the usual three points of energy conservation. High-amplitude swelling and collapse
of the membrane potential were used as parameters for demonstrating induction of the mitochondrial permeability transition
due to opening of a pore (mPTP). Mitochondria from Y. lipolytica, lacking a natural mitochondrial Ca2+ uptake pathway, and from D. magnusii, harboring a high-capacitive, regulated mitochondrial Ca2+ transport system (Bazhenova et al. J Biol Chem 273:4372–4377, 1998a; Bazhenova et al. Biochim Biophys Acta 1371:96–100, 1998b; Deryabina and Zvyagilskaya Biochemistry (Moscow) 65:1352–1356, 2000; Deryabina et al. J Biol Chem 276:47801–47806, 2001) were very resistant to Ca2+ overload. However, exposure of yeast mitochondria to 50–100 μM Ca2+ in the presence of the Ca2+ ionophore ETH129 induced collapse of the membrane potential, possibly due to activation of the fatty acid-dependent Ca2+/nH+-antiporter, with no classical mPTP induction. The absence of response in yeast mitochondria was not simply due to structural
limitations, since large-amplitude swelling occurred in the presence of alamethicin, a hydrophobic, helical peptide, forming
voltage-sensitive ion channels in lipid membranes. Ca2+- ETH129-induced activation of the Ca2+/H+-antiport system was inhibited and prevented by bovine serum albumin, and partially by inorganic phosphate and ATP. We subjected
yeast mitochondria to other conditions known to induce the permeability transition in animal mitochondria, i.e., Ca2+ overload (in the presence of ETH129) combined with palmitic acid (Mironova et al. J Bioenerg Biomembr 33:319–331, 2001; Sultan and Sokolove Arch Biochem Biophys 386:37–51, 2001), SH-reagents, carboxyatractyloside (an inhibitor of the ADP/ATP translocator), depletion of intramitochondrial adenine nucleotide
pools, deenergization of mitochondria, and shifting to acidic pH values in the presence of high phosphate concentrations.
None of the above-mentioned substances or conditions induced a mPTP-like pore. It is thus evident that the permeability transition
in yeast mitochondria is not coupled with Ca2+ uptake and is differently regulated compared to the mPTP of animal mitochondria. 相似文献
7.
《Cell calcium》2018
The KRAS GTPase plays a fundamental role in transducing signals from plasma membrane growth factor receptors to downstream signalling pathways controlling cell proliferation, survival and migration. Activating KRAS mutations are found in 20% of all cancers and in up to 40% of colorectal cancers, where they contribute to dysregulation of cell processes underlying oncogenic transformation. Multiple KRAS-regulated cell functions are also influenced by changes in intracellular Ca2+ levels that are concurrently modified by receptor signalling pathways. Suppression of intracellular Ca2+ release mechanisms can confer a survival advantage in cancer cells, and changes in Ca2+ entry across the plasma membrane modulate cell migration and proliferation. However, inconsistent remodelling of Ca2+ influx and its signalling role has been reported in studies of transformed cells. To isolate the interaction between altered Ca2+ handling and mutated KRAS in colorectal cancer, we have previously employed isogenic cell line pairs, differing by the presence of an oncogenic KRAS allele (encoding KRASG13D), and have shown that reduced Ca2+ release from the ER and mitochondrial Ca2+ uptake contributes to the survival advantage conferred by oncogenic KRAS. Here we show in the same cell lines, that Store-Operated Ca2+ Entry (SOCE) and its underlying current, ICRAC are under the influence of KRASG13D. Specifically, deletion of the oncogenic KRAS allele resulted in enhanced STIM1 expression and greater Ca2+ influx. Consistent with the role of KRAS in the activation of the ERK pathway, MEK inhibition in cells with KRASG13D resulted in increased STIM1 expression. Further, ectopic expression of STIM1 in HCT 116 cells (which express KRASG13D) rescued SOCE, demonstrating a fundamental role of STIM1 in suppression of Ca2+ entry downstream of KRASG13D. These results add to the understanding of how ERK controls cancer cell physiology and highlight STIM1 as an important biomarker in cancerogenesis. 相似文献
8.
《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》2023,1870(7):119532
Apoptosis is a highly complex and regulated cell death pathway that safeguards the physiological balance between life and death. Over the past decade, the role of Ca2+ signalling in apoptosis and the mechanisms involved have become clearer. The initiation and execution of apoptosis is coordinated by three distinct groups of cysteines proteases: the caspase, calpain and cathepsin families. Beyond its physiological importance, the ability to evade apoptosis is a prominent hallmark of cancer cells. In this review, we will explore the involvement of Ca2+ in the regulation of caspase, calpain and cathepsin activity, and how the actions of these cysteine proteases alter intracellular Ca2+ handling during apoptosis. We will also explore how apoptosis resistance can be achieved in cancer cells through deregulation of cysteine proteases and remodelling of the Ca2+ signalling toolkit. 相似文献
9.
《Cell calcium》2019
Cancer stem cells are a subpopulation of tumor cells that proliferate, self-renew and produce more differentiated tumoral cells building-up the tumor. Responsible for the sustained growth of malignant tumors, cancer stem cells are proposed to play significant roles in cancer resistance to standard treatment and in tumor recurrence. Among the mechanisms dysregulated in neoplasms, those related to Ca2+ play significant roles in various aspects of cancers. Ca2+ is a ubiquitous second messenger whose fluctuations of its intracellular concentrations are tightly controlled by channels, pumps, exchangers and Ca2+ binding proteins. These components support the genesis of Ca2+ signals with specific spatio-temporal characteristics that define the cell response. Being involved in the coupling of extracellular events with intracellular responses, the Ca2+ toolkit is often hijacked by cancer cells to promote notably their proliferation and invasion. Growing evidence obtained during the last decade pointed to a role of Ca2+ handling and mishandling in cancer stem cells. In this review, after a general overview of the concept of cancer stem cells we analyse and discuss the studies and current knowledge regarding the complex roles of Ca2+ toolkit and signaling in these cells. We highlight that numbers of Ca2+ signaling actors promote cancer stem cell state and are associated with cell resistance to current cancer treatments and thus may represent promising targets for potential clinical applications. 相似文献
10.
Clark W. Distelhorst 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》2018,1865(11):1795-1804
Bcl-2 inhibits cell death by at least two different mechanisms. On the one hand, its BH3 domain binds to pro-apoptotic proteins such as Bim and prevents apoptosis induction. On the other hand, the BH4 domain of Bcl-2 binds to the inositol 1,4,5-trisphosphate receptor (IP3R), preventing Ca2+ signals that mediate cell death. In normal T-cells, Bcl-2 levels increase during the immune response, protecting against cell death, and then decline as apoptosis ensues and the immune response dissipates. But in many cancers Bcl-2 is aberrantly expressed and exploited to prevent cell death by inhibiting IP3R-mediated Ca2+ elevation. This review summarizes what is known about the mechanism of Bcl-2's control over IP3R-mediated Ca2+ release and cell death induction. Early insights into the role of Ca2+ elevation in corticosteroid-mediated cell death serves as a model for how targeting IP3R-mediated Ca2+ elevation can be a highly effective therapeutic approach for different types of cancer. Moreover, the successful development of ABT-199 (Venetoclax), a small molecule targeting the BH3 domain of Bcl-2 but without effects on Ca2+, serves as proof of principle that targeting Bcl-2 can be an effective therapeutic approach. BIRD-2, a synthetic peptide that inhibits Bcl-2-IP3R interaction, induces cell death induction in ABT-199 (Venetoclax)-resistant cancer models, attesting to the value of developing therapeutic agents that selectively target Bcl-2-IP3R interaction, inducing Ca2+-mediated cell death. 相似文献
11.
Camperi and Wang (Comput Neurosci 5:383–405, 1998) presented a network model for working memory that combines intrinsic cellular bistability with the recurrent network architecture
of the neocortex. While Fall and Rinzel (Comput Neurosci 20:97–107, 2006) replaced this intrinsic bistability with a biological mechanism-Ca2+ release subsystem. In this study, we aim to further expand the above work. We integrate the traditional firing-rate network
with Ca2+ subsystem-induced bistability, amend the synaptic weights and suggest that Ca2+ concentration only increase the efficacy of synaptic input but has nothing to do with the external input for the transient
cue. We found that our network model maintained the persistent activity in response to a brief transient stimulus like that
of the previous two models and the working memory performance was resistant to noise and distraction stimulus if Ca2+ subsystem was tuned to be bistable. 相似文献
12.
Nikolay K. Isaev Elena V. Stelmashook Sergey V. Lukin Dorette Freyer Philipp Mergenthaler Dmitry B. Zorov 《Cellular and molecular neurobiology》2010,30(6):877-883
Severe acidosis caused death of cultured cerebellar granule neurons (CGNs). Acidosis was accompanied by a progressive increase
of the intracellular zinc ions ([Zn2+]i) and decrease of [Ca2+]i. Zn2+ chelator, N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), prevented the increase of [Zn2+]i and acidosis-induced neuronal death. However, neuronal death was insensitive to blockade of ASIC1 channels with amiloride,
as CGNs display considerably lower expression of ASIC1a than other neurons. The antioxidant trolox and menadione significantly
protected neurons from acidotic death. Earlier, we demonstrated that menadione rescues neurons from the deleterious effect
of inhibition of mitochondrial complex I (Isaev et al. Neuroreport 15:2227–2231, 2004). We speculate that excessive Zn2+-dependent production of reactive oxygen species by mitochondrial complex I may be a general motive for the induction of cell
death in CGNs under acidotic conditions. 相似文献
13.
Elongation growth rate of stem cells of Impatiens balsamina was inhibited by the heavy metals Pb2+, Cd2+ and Zn2+ due to their suppression on cell wall extensibility. Effective turgor was also inhibited by Pb2+ and Cd2+ but it played a secondary role in reducing the stem cell elongation growth rate. The major rate-limiting factor for cell elongation growth was the cell wall extensibility. Furthermore, Cd2+ was found to be more toxic than Pb2+, while Pb2+ was more toxic than Zn2+. 相似文献
14.
Powered by the mitochondrial membrane potential, Ca2+ permeates the mitochondria via a Ca2+ channel termed Ca2+ uniporter and is pumped out by a Na+/Ca2+ exchanger, both of which are located on the inner mitochondrial membrane. Mitochondrial Ca2+ transients are critical for metabolic activity and regulating global Ca2+ responses. On the other hand, failure to control mitochondrial Ca2+ is a hallmark of ischemic and neurodegenerative diseases. Despite their importance, identifying the uniporter and exchanger remains elusive and their inhibitors are non-specific. This review will focus on the mitochondrial exchanger, initially describing how it was molecularly identified and linked to a novel member of the Na+/Ca2+ exchanger superfamily termed NCLX. Molecular control of NCLX expression provides a selective tool to determine its physiological role in a variety of cell types. In lymphocytes, NCLX is essential for refilling the endoplasmic reticulum Ca2+ stores required for antigendependent signaling. Communication of NCLX with the store-operated channel in astroglia controls Ca2+ influx and thereby neuro-transmitter release and cell proliferation. The refilling of the Ca2+ stores in the sarcoplasmic reticulum, which is controlled by NCLX, determines the frequency of action potential and Ca2+ transients in cardiomyocytes. NCLX is emerging as a hub for integrating glucose-dependent Na+ and Ca2+ signaling in pancreatic β cells, and the specific molecular control of NCLX expression resolved the controversy regarding its role in neurons and β cells. Future studies on an NCLX knockdown mouse model and identification of human NCLX mutations are expected to determine the role of mitochondrial Ca2+ efflux in organ activity and whether NCLX inactivation is linked to ischemic and/or neurodegenerative syndromes. Structure-function analysis and protein analysis will identify the NCLX mode of regulation and its partners in the inner membrane of the mitochondria. 相似文献
15.
F. Vanden Abeele Y. Shuba M. Roudbaraki L. Lemonnier K. Vanoverberghe P. Mariot R. Skryma N. Prevarskaya 《Cell calcium》2003,33(5-6):357
Ca2+ homeostasis mechanisms, in which the Ca2+ entry pathways play a key role, are critically involved in both normal function and cancerous transformation of prostate epithelial cells. Here, using the lymph node carcinoma of the prostate (LNCaP) cell line as a major experimental model, we characterize prostate-specific store-operated Ca2+ channels (SOCs)—a primary Ca2+ entry pathway for non-excitable cells—for the first time. We show that prostate-specific SOCs share major store-dependent, kinetic, permeation, inwardly rectifying, and pharmacological (including dual, potentiation/inhibition concentration-dependent sensitivity to 2-APB) properties with “classical” Ca2+ release-activated Ca2+ channels (CRAC), but have a higher single channel conductance (3.2 and 12 pS in Ca2+- and Na+-permeable modes, respectively). They are subject to feedback inhibition via Ca2+-dependent PKC, CaMK-II and CaM regulatory pathways and are functionally dependent on caveolae integrity. Caveolae also provide a scaffold for spatial co-localization of SOCs with volume-regulated anion channels (VRAC) and their Ca2+-mediated interaction. The TRPC1 and TRPV6 members of the transient receptor potential (TRP) channel family are the most likely molecular candidates for the formation of prostate-specific endogenous SOCs. Differentiation of LNCaP cells to an androgen-insensitive, apoptotic-resistant neuroendocrine phenotype downregulates SOC current. We conclude that prostate-specific SOCs are important determinants in the transition to androgen-independent prostate cancer. 相似文献
16.
Nicolás Veiga Julia Torres Himali Y. Godage Andrew M. Riley Sixto Domínguez Barry V. L. Potter Alvaro Díaz Carlos Kremer 《Journal of biological inorganic chemistry》2009,14(7):1001-1013
The inositol phosphates are ubiquitous metabolites in eukaryotes, of which the most abundant are inositol hexakisphosphate
(InsP
6) and inositol 1,3,4,5,6-pentakisphosphate [Ins(1,3,4,5,6)P
5)]. These two compounds, poorly understood functionally, have complicated complexation and solid formation behaviours with
multivalent cations. For InsP
6, we have previously described this chemistry and its biological implications (Veiga et al. in J Inorg Biochem 100:1800, 2006; Torres et al. in J Inorg Biochem 99:828, 2005). We now cover similar ground for Ins(1,3,4,5,6)P
5, describing its interactions in solution with Na+, K+, Mg2+, Ca2+, Cu2+, Fe2+ and Fe3+, and its solid-formation equilibria with Ca2+ and Mg2+. Ins(1,3,4,5,6)P
5 forms soluble complexes of 1:1 stoichiometry with all multivalent cations studied. The affinity for Fe3+ is similar to that of InsP
6 and inositol 1,2,3-trisphosphate, indicating that the 1,2,3-trisphosphate motif, which Ins(1,3,4,5,6)P
5 lacks, is not absolutely necessary for high-affinity Fe3+ complexation by inositol phosphates, even if it is necessary for their prevention of the Fenton reaction. With excess Ca2+ and Mg2+, Ins(1,3,4,5,6)P
5 also forms the polymetallic complexes [M4(H2L)] [where L is fully deprotonated Ins(1,3,4,5,6)P
5]. However, unlike InsP
6, Ins(1,3,4,5,6)P
5 is predicted not to be fully associated with Mg2+ under simulated cytosolic/nuclear conditions. The neutral Mg2+ and Ca2+ complexes have significant windows of solubility, but they precipitate as [Mg4(H2L)]·23H2O or [Ca4(H2L)]·16H2O whenever they exceed 135 and 56 μM in concentration, respectively. Nonetheless, the low stability of the [M4(H2L)] complexes means that the 1:1 species contribute to the overall solubility of Ins(1,3,4,5,6)P
5 even under significant Mg2+ or Ca2+ excesses. We summarize the solubility behaviour of Ins(1,3,4,5,6)P
5 in straightforward plots. 相似文献
17.
Podchanart Wanitchakool Luisa Wolf Gudrun E. Koehl Lalida Sirianant Rainer Schreiber Sucheta Kulkarni Umamaheswar Duvvuri Karl Kunzelmann 《Philosophical transactions of the Royal Society of London. Series B, Biological sciences》2014,369(1638)
Anoctamin 1 (TMEM16A, Ano1) is a recently identified Ca2+-activated chloride channel and a member of a large protein family comprising 10 paralogues. Before Ano1 was identified as a chloride channel protein, it was known as the cancer marker DOG1. DOG1/Ano1 is expressed in gastrointestinal stromal tumours (GIST) and particularly in head and neck squamous cell carcinoma, at very high levels never detected in other tissues. It is now emerging that Ano1 is part of the 11q13 locus, amplified in several types of tumour, where it is thought to augment cell proliferation, cell migration and metastasis. Notably, Ano1 is upregulated through histone deacetylase (HDAC), corresponding to the known role of HDAC in HNSCC. As Ano1 does not enhance proliferation in every cell type, its function is perhaps modulated by cell-specific factors, or by the abundance of other anoctamins. Thus Ano6, by regulating Ca2+-induced membrane phospholipid scrambling and annexin V binding, supports cellular apoptosis rather than proliferation. Current findings implicate other cellular functions of anoctamins, apart from their role as Ca2+-activated Cl− channels. 相似文献
18.
Avilés C Torres-Márquez ME Mendoza-Cózatl D Moreno-Sánchez R 《Archives of microbiology》2005,184(2):83-92
To determine the onset of the Cd2+-hyperaccumulating phenotype in Euglena gracilis, induced by Hg2+ pretreatment (Avilés et al. in Arch Microbiol 180:1–10, 2003), the changes in cellular growth, Cd2+ uptake, and intracellular contents of sulfide, cysteine, γ-glutamylcysteine, glutathione and phytochelatins during the progress
of the culture were analyzed. In cells exposed to 0.2 mM CdCl2, the Cd2+-hyperaccumulating phenotype was apparent only after 48 h of culture, as indicated by the significant increase in cell growth
and higher internal contents of sulfide and thiol-compounds, along with a higher γ-glutamylcysteine synthetase activity. However,
the stiochiometry of thiol-compounds/Cd2+ accumulated was similar for both control and Hg2+-pretreated cells. Moreover, the value for this ratio was 2.1 or lower after 48-h culture, which does not suffice to fully
inactivate Cd2+. It is concluded that, although the glutathione and phytochelatin synthesis pathway is involved in the development of the
Cd2+-hyperaccumulating phenotype in E. gracilis, apparently other pathways and sub-cellular mechanisms are also involved. These may be an increase in other Cd2+ chelating molecules such as di- and tricarboxylic acids, phosphate and polyphosphates, as well as Cd2+ compartmentation into organelles.
César Avilés: In memoriam. 相似文献
19.
Roman Przymusiński Renata Rucińska-Sobkowiak Bogna Ilska Edward A. Gwóźdź 《Acta Physiologiae Plantarum》2007,29(5):411-416
In an earlier work using tissue printing method, we found that the PR-10 stress protein was observed in leaf petiole of lupin
seedling where lead was not detected (Przymusiński et al. 2001). These results suggested the presence of substance(s) mediating a signal transduction from directly affected cells to distant
organs. As the hydrogen peroxide was found to be involved in signal transduction pathway, in the present paper, we analysed
the level of H2O2 in the organ of lupin seedlings exposed to Pb2+ with spectrophotometric method and tissue printing technique. It was unequivocally demonstrated that the level of H2O2 and the activity of peroxidase increased in every tested organ of lead-treated lupin seedling. Both the level of H2O2 and the activity of POX were correlated with amount of Pb2+ ions in the cells (Przymusiński et al. 2001) and decreased in tissues more and more distant from the site of metal application. On the other hand, there was no correlation
between the histological localization of H2O2 and peroxidase. Our results seem to confirm the hypothesis that H2O2 may act as a signalling substance involved in the induction of PR protein synthesis. It was indicated that there is high
degree of correlation between the localization of H2O2 and the histological localization of PR-10 proteins (Przymusiński et al. 2001) in every tested organ of lupin seedling. The presented hypothesis is also supported by the fact that H2O2 and PR-10 proteins are detected in organs and tissues where Pb2+ was not found at all. 相似文献
20.
Tat’yana Trendeleva Evgeniya Sukhanova Ludmila Ural’skaya Nils-Erik Saris Renata Zvyagilskaya 《Journal of bioenergetics and biomembranes》2011,43(6):623-631
In this study we used tightly-coupled mitochondria from Yarrowia lipolytica and Dipodascus (Endomyces) magnusii yeasts. The two yeast strains are good alternatives to Saccharomyces cerevisiae, being aerobes containing well-structured mitochondria (thus ensuring less structural limitation to observe their appreciable
swelling) and fully competent respiratory chain with three invariantly functioning energy conservation points, including Complex
I, that can be involved in induction of the canonical Ca2+/Pi-dependent mitochondrial permeability transition (mPTP pore) with an increased open probability when electron flux increases
(Fontaine et al. J Biol Chem 273:25734–25740, 1998; Bernardi et al. FEBS J 273:2077–2099, 2006). High-amplitude swelling and collapse of the membrane potential were used as parameters for demonstrating pore opening.
Previously (Kovaleva et al. J Bioenerg Biomembr 41:239–249, 2009; Kovaleva et al. Biochemistry (Moscow) 75:297–303, 2010) we have shown that mitochondria from Y. lipolytica and D. magnusii were very resistant to the Ca2+ overload combined with varying concentrations of Pi, palmitic acid, SH-reagents, carboxyatractyloside (an inhibitor of ADP/ATP translocator), as well as depletion of intramitochondrial
adenine nucleotide pools, deenergization of mitochondria, and shifting to acidic pH values in the presence of high [Pi]. Here we subjected yeast mitochondria to other conditions known to induce an mPTP in animal and plant mitochondria, namely
to Ca2+ overload under hypoxic conditions (anaerobiosis). We were unable to observe Ca2+-induced high permeability of the inner membrane of D. magnusii and Y. lipolytica yeast mitochondria under anaerobic conditions, thus suggesting that an mPTP-like pore, if it ever occurs in yeast mitochondria,
is not coupled with the Ca2+ uptake. The results provide the first demonstration of ATP-dependent energization of yeast mitochondria under conditions
of anaerobiosis. 相似文献