BACKGROUND: The unfolded protein response (UPR) enables myeloma cells to overcome the stress conditions arising from excessive proteosynthesis and thus provides a survival advantage for myeloma cells. Extramedullary disease is a more aggressive form of multiple myeloma in which myeloma cells lose their dependence on the bone marrow microenvironment and are able to infiltrate other tissues and organs. The pathogenesis of extramedullary disease is not fully elucidated yet. The aim of this study was to determine whether there is a difference in the expression of UPR-related genes between bone marrow plasma cells from multiple myeloma and extramedullary disease patients. MATERIALS AND METHODS: Gene expression of six genes involved in UPR (ERN1, DDIT3, EIF2AK3, TUSC3, XBP1, HSPA5) was analyzed by quantitative reverse transcription polymerase chain reaction. In total, 76 bone marrow plasma cell samples were used, of which 44 were from patients with multiple myeloma and 32 from patients with extramedullary disease. RESULTS: A statistically significant difference was observed between the multiple myeloma and extramedullary disease groups regarding the expression of HSPA5, DDIT3, EIF2AK3, and ERN1 genes. However, in the case of XBP1 and TUSC3 genes, no statistically significant difference in the expression was found. Several statistically significant correlations between the expression levels of the analyzed genes and the clinical data of the patients were observed as well. CONCLUSION: Our results suggest the importance of UPR in the pathogenesis of extramedullary disease. UPR appears to be a promising avenue for further research.

• Klíčová slova
• Kahler-Pick law, Multiple myeloma, Plasma cells, extramedullary disease, unfolded protein response,
• MeSH
• chaperon endoplazmatického retikula BiP MeSH
• endoribonukleasy genetika   MeSH
• kinasa eIF-2 MeSH
• lidé středního věku MeSH
• lidé MeSH
• mnohočetný myelom * genetika   metabolismus   patologie   MeSH
• plazmatické buňky metabolismus   MeSH
• protein-serin-threoninkinasy genetika   MeSH
• proteiny teplotního šoku genetika   MeSH
• senioři MeSH
• signální dráha UPR * genetika   MeSH
• transkripční faktor CHOP genetika   MeSH
• transkripční faktory RFX MeSH
• XBP1 genetika   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• chaperon endoplazmatického retikula BiP MeSH
• DDIT3 protein, human MeSH Prohlížeč
• EIF2AK3 protein, human MeSH Prohlížeč
• endoribonukleasy MeSH
• ERN1 protein, human MeSH Prohlížeč
• HSPA5 protein, human MeSH Prohlížeč
• kinasa eIF-2 MeSH
• protein-serin-threoninkinasy MeSH
• proteiny teplotního šoku MeSH
• transkripční faktor CHOP MeSH
• transkripční faktory RFX MeSH
• XBP1 protein, human MeSH Prohlížeč
• XBP1 MeSH

Adar null mutant mouse embryos die with aberrant double-stranded RNA (dsRNA)-driven interferon induction, and Adar Mavs double mutants, in which interferon induction is prevented, die soon after birth. Protein kinase R (Pkr) is aberrantly activated in Adar Mavs mouse pup intestines before death, intestinal crypt cells die, and intestinal villi are lost. Adar Mavs Eifak2 (Pkr) triple mutant mice rescue all defects and have long-term survival. Adenosine deaminase acting on RNA 1 (ADAR1) and PKR co-immunoprecipitate from cells, suggesting PKR inhibition by direct interaction. AlphaFold studies on an inhibitory PKR dsRNA binding domain (dsRBD)-kinase domain interaction before dsRNA binding and on an inhibitory ADAR1 dsRBD3-PKR kinase domain interaction on dsRNA provide a testable model of the inhibition. Wild-type or editing-inactive human ADAR1 expressed in A549 cells inhibits activation of endogenous PKR. ADAR1 dsRNA binding is required for, but is not sufficient for, PKR inhibition. Mutating the ADAR1 dsRBD3-PKR contact prevents co-immunoprecipitation, ADAR1 inhibition of PKR activity, and co-localization of ADAR1 and PKR in cells.

• Klíčová slova
• ADAR RNA editing, Adar mutant, Aicardi-Goutieres Syndrome (AGS), CP: Molecular biology, Mavs, dsRNA, dsRNA-binding protein, innate immune sensors, protein kinase R,
• MeSH
• adenosindeaminasa * metabolismus   genetika   MeSH
• aktivace enzymů MeSH
• buňky A549 MeSH
• dvouvláknová RNA * metabolismus   MeSH
• kinasa eIF-2 * metabolismus   MeSH
• lidé MeSH
• myši MeSH
• proteinové domény MeSH
• proteiny vázající RNA * metabolismus   genetika   MeSH
• vazba proteinů MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• ADAR protein, human MeSH Prohlížeč
• adenosindeaminasa * MeSH
• dvouvláknová RNA * MeSH
• kinasa eIF-2 * MeSH
• proteiny vázající RNA * MeSH

The TcK2 protein kinase of Trypanosoma cruzi, the causative agent of Chagas disease, is structurally similar to the human kinase PERK, which phosphorylates the initiation factor eIF2α and, in turn, inhibits translation initiation. We have previously shown that absence of TcK2 kinase impairs parasite proliferation within mammalian cells, positioning it as a potential target for treatment of Chagas disease. To better understand its role in the parasite, here we initially confirmed the importance of TcK2 in parasite proliferation by generating CRISPR/Cas9 TcK2-null cells, albeit they more efficiently differentiate into infective forms. Proteomics indicates that the TcK2 knockout of proliferative forms expresses proteins including trans-sialidases, normally restricted to infective and nonproliferative trypomastigotes explaining decreased proliferation and better differentiation. TcK2 knockout cells lost phosphorylation of eukaryotic initiation factor 3 and cyclic AMP responsive-like element, recognized to promote growth, likely explaining both decreased proliferation and augmented differentiation. To identify specific inhibitors, a library of 379 kinase inhibitors was screened by differential scanning fluorimetry using a recombinant TcK2 encompassing the kinase domain and selected molecules were tested for kinase inhibition. Only Dasatinib and PF-477736, inhibitors of Src/Abl and ChK1 kinases, showed inhibitory activity with IC50 of 0.2 ± 0.02 mM and 0.8 ± 0.1, respectively. In infected cells Dasatinib inhibited growth of parental amastigotes (IC50 = 0.6 ± 0.2 mM) but not TcK2 of depleted parasites (IC50 > 34 mM) identifying Dasatinib as a potential lead for development of therapeutics for Chagas disease targeting TcK2.

• Klíčová slova
• T.cruzi EIF2AK2, chagas disease, chemical inhibitor, eIF2α, invasion, protein kinase, proteome, recombinant protein,
• MeSH
• Chagasova nemoc * farmakoterapie   parazitologie   MeSH
• dasatinib MeSH
• kinasa eIF-2 genetika   metabolismus   MeSH
• lidé MeSH
• paraziti * MeSH
• proliferace buněk MeSH
• savci metabolismus   MeSH
• Trypanosoma cruzi * genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• dasatinib MeSH
• kinasa eIF-2 MeSH

Cellular stress conditions activate p53-dependent pathways to counteract the inflicted damage. To achieve the required functional diversity, p53 is subjected to numerous post-translational modifications and the expression of isoforms. Little is yet known how p53 has evolved to respond to different stress pathways. The p53 isoform p53/47 (p47 or ΔNp53) is linked to aging and neural degeneration and is expressed in human cells via an alternative cap-independent translation initiation from the 2nd in-frame AUG at codon 40 (+118) during endoplasmic reticulum (ER) stress. Despite an AUG codon in the same location, the mouse p53 mRNA does not express the corresponding isoform in either human or mouse-derived cells. High-throughput in-cell RNA structure probing shows that p47 expression is attributed to PERK kinase-dependent structural alterations in the human p53 mRNA, independently of eIF2α. These structural changes do not take place in murine p53 mRNA. Surprisingly, PERK response elements required for the p47 expression are located downstream of the 2nd AUG. The data show that the human p53 mRNA has evolved to respond to PERK-mediated regulation of mRNA structures in order to control p47 expression. The findings highlight how p53 mRNA co-evolved with the function of the encoded protein to specify p53-activities under different cellular conditions.

• MeSH
• kinasa eIF-2 genetika   metabolismus   MeSH
• lidé MeSH
• messenger RNA genetika   metabolismus   MeSH
• myši MeSH
• nádorový supresorový protein p53 * genetika   metabolismus   MeSH
• posttranslační úpravy proteinů MeSH
• protein - isoformy metabolismus   MeSH
• stres endoplazmatického retikula * genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• kinasa eIF-2 MeSH
• messenger RNA MeSH
• nádorový supresorový protein p53 * MeSH
• protein - isoformy MeSH

RNAi is the sequence-specific mRNA degradation guided by siRNAs produced from long dsRNA by RNase Dicer. Proteins executing RNAi are present in mammalian cells but rather sustain the microRNA pathway. Aiming for a systematic analysis of mammalian RNAi, we report here that the main bottleneck for RNAi efficiency is the production of functional siRNAs, which integrates Dicer activity, dsRNA structure, and siRNA targeting efficiency. Unexpectedly, increased expression of Dicer cofactors TARBP2 or PACT reduces RNAi but not microRNA function. Elimination of protein kinase R, a key dsRNA sensor in the interferon response, had minimal positive effects on RNAi activity in fibroblasts. Without high Dicer activity, RNAi can still occur when the initial Dicer cleavage of the substrate yields an efficient siRNA. Efficient mammalian RNAi may use substrates with some features of microRNA precursors, merging both pathways even more than previously suggested. Although optimized endogenous Dicer substrates mimicking miRNA features could evolve for endogenous regulations, the same principles would make antiviral RNAi inefficient as viruses would adapt to avoid efficacy.

• MeSH
• buňky NIH 3T3 MeSH
• DEAD-box RNA-helikasy metabolismus   MeSH
• dvouvláknová RNA genetika   metabolismus   MeSH
• genový knockout MeSH
• kinasa eIF-2 genetika   MeSH
• malá interferující RNA metabolismus   MeSH
• mikro RNA metabolismus   MeSH
• myši MeSH
• plazmidy genetika   MeSH
• proteiny vázající RNA metabolismus   MeSH
• ribonukleasa III metabolismus   MeSH
• RNA interference fyziologie   MeSH
• sekvence nukleotidů genetika   MeSH
• transfekce MeSH
• transportní proteiny metabolismus   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• DEAD-box RNA-helikasy MeSH
• Dicer1 protein, mouse MeSH Prohlížeč
• dvouvláknová RNA MeSH
• kinasa eIF-2 MeSH
• malá interferující RNA MeSH
• mikro RNA MeSH
• protein kinase R, mouse MeSH Prohlížeč
• proteiny vázající RNA MeSH
• Rbbp6 protein, mouse MeSH Prohlížeč
• ribonukleasa III MeSH
• trans-activation responsive RNA-binding protein MeSH Prohlížeč
• transportní proteiny MeSH

The integrated stress response (ISR) is a homeostatic mechanism induced by endoplasmic reticulum (ER) stress. In acute/transient ER stress, decreased global protein synthesis and increased uORF mRNA translation are followed by normalization of protein synthesis. Here, we report a dramatically different response during chronic ER stress. This chronic ISR program is characterized by persistently elevated uORF mRNA translation and concurrent gene expression reprogramming, which permits simultaneous stress sensing and proteostasis. The program includes PERK-dependent switching to an eIF3-dependent translation initiation mechanism, resulting in partial, but not complete, translational recovery, which, together with transcriptional reprogramming, selectively bolsters expression of proteins with ER functions. Coordination of transcriptional and translational reprogramming prevents ER dysfunction and inhibits "foamy cell" development, thus establishing a molecular basis for understanding human diseases associated with ER dysfunction.

• Klíčová slova
• ER stress, PERK, eIF2, eIF2B, eIF3, integrated stress response, mRNA translation, protein synthesis, stress signaling, unfolded protein response,
• MeSH
• časové faktory MeSH
• eukaryotický iniciační faktor 3 genetika   metabolismus   MeSH
• fenotyp MeSH
• fibroblasty metabolismus   patologie   MeSH
• genetická transkripce * MeSH
• HEK293 buňky MeSH
• homeostáze proteinů MeSH
• kinasa eIF-2 genetika   metabolismus   MeSH
• lidé MeSH
• messenger RNA biosyntéza   genetika   MeSH
• myši MeSH
• otevřené čtecí rámce MeSH
• přeprogramování buněk MeSH
• proteosyntéza * MeSH
• RNA interference MeSH
• signální transdukce MeSH
• stres endoplazmatického retikula * MeSH
• transfekce MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• eukaryotický iniciační faktor 3 MeSH
• kinasa eIF-2 MeSH
• messenger RNA MeSH
• PERK kinase MeSH Prohlížeč

Chronic exposure to trichothecenes is known to disturb insulin-like growth factor 1 and signaling of insulin and leptin hormones and causes considerable growth retardation in animals. However, limited information was available on mechanisms underlying trichothecene-induced growth retardation. In this study, we employed an integrated transcriptomics, proteomics, and RNA interference (RNAi) approach to study the molecular mechanisms underlying trichothecene cytotoxicity in rat pituitary adenoma GH3 cells. Our results showed that trichothecenes suppressed the synthesis of growth hormone 1 (Gh1) and inhibited the eukaryotic transcription and translation initiation by suppressing aminoacyl-tRNA synthetases transcription, inducing eukaryotic translation initiation factor 2-alpha kinase 2 (EIF2AK2) and reducing eukaryotic translation initiation factor 5 a. The sulfhydryl oxidases , protein disulfide isomerase,and heat shock protein 90 (were greatly reduced, which resulted in adverse regulation of protein processing and folding. Differential genes and proteins associated with a decline in energy metabolism and cell cycle arrest were also found in our study. However, use of RNAi to interfere with hemopoietic cell kinase (Hck) and EIF2AK2 transcriptions or use of chemical inhibitors of MAPK, p38, Ras, and JNK partially reversed the reduction of Gh1 levels induced by trichothecenes. It indicated that the activation of MAPKs, Hck, and EIF2AK2 were important for trichothecene-induced growth hormone suppression. Considering the potential hazards of exposure to trichothecenes, our findings could help to improve our understanding regarding human and animal health implications.

• Klíčová slova
• EIF2AK2, Gh1, Hck, growth retardation, trichothecene,
• MeSH
• aminoacyl-tRNA-synthetasy antagonisté a inhibitory   MeSH
• apoptóza účinky léků   MeSH
• buněčné linie MeSH
• eukaryotický translační iniciační faktor 5A MeSH
• genetická transkripce účinky léků   MeSH
• iniciační faktory antagonisté a inhibitory   MeSH
• kinasa eIF-2 antagonisté a inhibitory   MeSH
• krysa rodu Rattus MeSH
• oxidoreduktasy antagonisté a inhibitory   MeSH
• proteindisulfidisomerasy antagonisté a inhibitory   MeSH
• proteiny tepelného šoku HSP90 antagonisté a inhibitory   MeSH
• proteiny vázající RNA antagonisté a inhibitory   MeSH
• proteomika * MeSH
• proteosyntéza účinky léků   MeSH
• RNA interference účinky léků   MeSH
• růstový hormon antagonisté a inhibitory   MeSH
• stanovení celkové genové exprese * MeSH
• T-2 toxin analogy a deriváty   farmakologie   MeSH
• viabilita buněk účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• 4'-hydroxy T-2 toxin MeSH Prohlížeč
• aminoacyl-tRNA-synthetasy MeSH
• iniciační faktory MeSH
• kinasa eIF-2 MeSH
• oxidoreduktasy MeSH
• proteindisulfidisomerasy MeSH
• proteiny tepelného šoku HSP90 MeSH
• proteiny vázající RNA MeSH
• růstový hormon MeSH
• sulfhydryl oxidase MeSH Prohlížeč
• T-2 toxin MeSH

Tributyltin (TBT) is a ubiquitous contaminant in aquatic environment, but the detailed mechanisms underlying the toxicity of TBT have not been fully understood. In this study, the effects of TBT on behavior, energy metabolism and endoplasmic reticulum (ER) stress were investigated by using Chinese rare minnow larvae. Fish larvae were exposed at sublethal concentrations of TBT (100, 400 and 800 ng/L) for 7 days. Compared with the control, energy metabolic parameters (RNA/DNA ratio, Na(+)-K(+)-ATPase) were significantly inhibited in fish exposed at highest concentration (800 ng/L), as well as abnormal behaviors observed. Moreover, we found that the PERK (PKR-like ER kinase)-eIF2α (eukaryotic translation initiation factor 2α) pathway, as the main branch was activated by TBT exposure in fish larvae. In short, TBT-induced physiological, biochemical and molecular responses in fish larvae were reflected in parameters measured in this study, which suggest that these biomarkers could be used as potential indicators for monitoring organotin compounds present in aquatic environment.

• Klíčová slova
• Behavior, Endoplasmic reticulum stress, Energy metabolism, Fish, Tributyltin,
• MeSH
• chování zvířat účinky léků   MeSH
• Cyprinidae růst a vývoj   MeSH
• DNA vazebné proteiny genetika   metabolismus   MeSH
• endoribonukleasy genetika   metabolismus   MeSH
• energetický metabolismus účinky léků   MeSH
• kinasa eIF-2 genetika   metabolismus   MeSH
• larva účinky léků   metabolismus   MeSH
• stres endoplazmatického retikula účinky léků   MeSH
• transkripční faktor ATF4 genetika   metabolismus   MeSH
• transkripční faktory RFX MeSH
• transkripční faktory genetika   metabolismus   MeSH
• trialkylcínové sloučeniny toxicita   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Čína MeSH
• Názvy látek
• DNA vazebné proteiny MeSH
• endoribonukleasy MeSH
• kinasa eIF-2 MeSH
• transkripční faktor ATF4 MeSH
• transkripční faktory RFX MeSH
• transkripční faktory MeSH
• trialkylcínové sloučeniny MeSH
• tributyltin MeSH Prohlížeč

Docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid present in fish oil, may exert cytotoxic and/or cytostatic effects on colon cancer cells when applied individually or in combination with some anticancer drugs. Here we demonstrate a selective ability of subtoxic doses of DHA to enhance antiproliferative and apoptotic effects of clinically useful cytokine TRAIL (tumor necrosis factor-related apoptosis inducing ligand) in cancer but not normal human colon cells. DHA-mediated stimulation of TRAIL-induced apoptosis was associated with extensive engagement of mitochondrial pathway (Bax/Bak activation, drop of mitochondrial membrane potential, cytochrome c release), activation of endoplasmic reticulum stress response (CHOP upregulation, changes in PERK level), decrease of cellular inhibitor of apoptosis protein (XIAP, cIAP1) levels and significant changes in sphingolipid metabolism (intracellular levels of ceramides, hexosyl ceramides, sphingomyelines, sphingosines; HPLC/MS/MS). Interestingly, we found significant differences in representation of various classes of ceramides (especially C16:0, C24:1) between the cancer and normal colon cells treated with DHA and TRAIL, and suggested their potential role in the regulation of the cell response to the drug combination. These study outcomes highlight the potential of DHA for a new combination therapy with TRAIL for selective elimination of colon cancer cells via simultaneous targeting of multiple steps in apoptotic pathways.

• Klíčová slova
• Apoptosis, Colon cancer, Docosahexaenoic acid, Lipid metabolism, TRAIL,
• MeSH
• adenokarcinom genetika   metabolismus   patologie   MeSH
• apoptóza účinky léků   genetika   MeSH
• cytochromy c metabolismus   MeSH
• inhibitory apoptózy MeSH
• kinasa eIF-2 genetika   metabolismus   MeSH
• kyseliny dokosahexaenové farmakologie   MeSH
• lidé MeSH
• membránový potenciál mitochondrií účinky léků   MeSH
• mitochondrie účinky léků   metabolismus   MeSH
• nádorové buněčné linie MeSH
• nádory tračníku genetika   metabolismus   patologie   MeSH
• protein Bak genetika   metabolismus   MeSH
• protein TRAIL farmakologie   MeSH
• protein X asociovaný s bcl-2 genetika   metabolismus   MeSH
• regulace genové exprese u nádorů * MeSH
• sfingolipidy chemie   klasifikace   metabolismus   MeSH
• signální transdukce MeSH
• stres endoplazmatického retikula účinky léků   MeSH
• synergismus léků MeSH
• transkripční faktor CHOP genetika   metabolismus   MeSH
• X-vázaný inhibitor apoptózy genetika   metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• BAK1 protein, human MeSH Prohlížeč
• BAX protein, human MeSH Prohlížeč
• cytochromy c MeSH
• DDIT3 protein, human MeSH Prohlížeč
• EIF2AK3 protein, human MeSH Prohlížeč
• inhibitory apoptózy MeSH
• kinasa eIF-2 MeSH
• kyseliny dokosahexaenové MeSH
• protein Bak MeSH
• protein TRAIL MeSH
• protein X asociovaný s bcl-2 MeSH
• sfingolipidy MeSH
• TNFSF10 protein, human MeSH Prohlížeč
• transkripční faktor CHOP MeSH
• X-vázaný inhibitor apoptózy MeSH
• XIAP protein, human MeSH Prohlížeč

We have analyzed the molecular mechanisms of photoinduced cell death using porphyrins with similar structure differing only in the position of the ethylene glycol (EG) chain on the phenyl ring. Meta- and para-positioned EG chains targeted porphyrins to different subcellular compartments. After photoactivation, both types of derivatives induced death of tumor cells via reactive oxygen species (ROS). Para derivatives pTPP(EG)4 and pTPPF(EG)4 primarily accumulated in lysosomes activated the p38 MAP kinase cascade, which in turn induced the mitochondrial apoptotic pathway. In contrast, meta porphyrin derivative mTPP(EG)4 localized in the endoplasmic reticulum (ER) induced dramatic changes in Ca(2+) homeostasis manifested by Ca(2+) rise in the cytoplasm, activation of calpains and stress caspase-12 or caspase-4. ER stress developed into unfolded protein response. Immediately after irradiation the PERK pathway was activated through phosphorylation of PERK, eIF2α and induction of transcription factors ATF4 and CHOP, which regulate stress response genes. PERK knockdown and PERK deficiency protected cells against mTPP(EG)4-mediated apoptosis, confirming the causative role of the PERK pathway.

• MeSH
• apoptóza účinky léků   účinky záření   MeSH
• ethylenglykol chemie   MeSH
• fotochemoterapie * MeSH
• genový knockdown MeSH
• homeostáza účinky léků   účinky záření   MeSH
• iniciační kaspasy metabolismus   MeSH
• kaspasa 2 metabolismus   MeSH
• kinasa eIF-2 nedostatek   genetika   metabolismus   MeSH
• lidé MeSH
• mitogenem aktivované proteinkinasy p38 metabolismus   MeSH
• nádorové buněčné linie MeSH
• porfyriny chemie   farmakologie   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• signální transdukce účinky léků   účinky záření   MeSH
• stres endoplazmatického retikula účinky léků   účinky záření   MeSH
• subcelulární frakce účinky léků   metabolismus   účinky záření   MeSH
• vápník metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• CASP4 protein, human MeSH Prohlížeč
• ethylenglykol MeSH
• iniciační kaspasy MeSH
• kaspasa 2 MeSH
• kinasa eIF-2 MeSH
• mitogenem aktivované proteinkinasy p38 MeSH
• PERK kinase MeSH Prohlížeč
• porfyriny MeSH
• reaktivní formy kyslíku MeSH
• vápník MeSH