We review trialkyltin and triaryltin compounds, representing a class of organometallic compounds that function as nuclear retinoid X receptors (RXR) agonists due to their capability to bind to the ligand-binding domain of RXR subtypes and function as transcriptional activators. RXRs act predominantly as heterodimers with other nuclear receptors as permissive heterodimers with peroxisome proliferator-activated receptors, liver X receptors, farnesoid X receptor, pregnane X receptor and constitutive androstan receptor or as non-permissive heterodimer with vitamin D receptor, and as conditional heterodimers with retinoid receptors, and thyroid hormone receptors. RXR - "partner" receptor heterodimers are considered to be ligand-activated, DNA-binding, trans-acting, transcription-modulating proteins involved in a general molecular mechanism responsible for transcriptional responses in target genes. Tributyltin at even pico- or nanomolar concentrations may cause the superimposition of male genitalia on female in several aquatic organisms, since they are DNA-targeted, mitotic, and their actions are occurring through target gene(s)-mediated pathways. They may cause molecular interactions with reproductive system in mammals, and as potent environmental obesogens, they promote adipocyte differentiation. Organotin compounds become known also for their immunotoxicity, neurotoxicity, for their effects on reproduction and/or development. We also review effects of organotins with respect to levels and activities of hepatic P450s and aromatase activity.

• Klíčová slova
• Antiproliferative effects, Cytochrom P-450, Environmental obesogen, Ligand inducible transcription factor, Metabolism, Nuclear receptor, Organotin compounds, Retinoid X receptor, Toxicity,
• MeSH
• genetická transkripce MeSH
• látky znečišťující životní prostředí toxicita   MeSH
• lidé MeSH
• organocínové sloučeniny toxicita   MeSH
• retinoidní X receptory agonisté   MeSH
• transkripční faktory metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• látky znečišťující životní prostředí MeSH
• organocínové sloučeniny MeSH
• retinoidní X receptory MeSH
• transkripční faktory MeSH

Plasminogen activator inhibitor 1 (PAI-1) is a crucial serine protease inhibitor that prevents plasminogen activation by inhibiting tissue- and urokinase-type plasminogen activators (tPA, uPA). PAI-1 is well-known for its role in modulating hemocoagulation or extracellular matrix formation by inhibiting plasmin or matrix metalloproteinases, respectively. PAI-1 is induced by pro-inflammatory cytokines across various tissues, yet its regulation by ligand-activated transcription factors is partly disregarded. Therefore, we have attempted to summarize the current knowledge on the transcriptional regulation of PAI-1 expression by the most relevant xenobiotic and endocrine receptors implicated in modulating PAI-1 levels. This review aims to contribute to the understanding of the specific, often tissue-dependent regulation of PAI-1 and provide insights into the modulation of PAI-1 levels beyond its direct inhibition.

• Klíčová slova
• AhR, Aryl hydrocarbon receptor, ER, Estrogen receptor, GR, Glucocorticoid receptor, MR, Mineralocorticoid receptor, PR, PXR, Pregnane X receptor, Progesterone receptor, THR, Thyroid hormone receptor, VDR, Vitamin D receptor,
• MeSH
• inhibitor aktivátoru plazminogenu 1 * metabolismus   genetika   MeSH
• lidé MeSH
• ligandy MeSH
• regulace genové exprese * MeSH
• transkripční faktory metabolismus   genetika   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• inhibitor aktivátoru plazminogenu 1 * MeSH
• ligandy MeSH
• SERPINE1 protein, human MeSH Prohlížeč
• transkripční faktory MeSH

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a death ligand with selective antitumor activity. However, many primary tumors are TRAIL resistant. Previous studies reported that roscovitine, a cyclin-dependent kinase inhibitor, sensitized various solid cancer cells to TRAIL. We show that roscovitine and TRAIL demonstrate synergistic cytotoxicity in hematologic malignant cell lines and primary cells. Pretreatment of TRAIL-resistant leukemia cells with roscovitine induced enhanced cleavage of death-inducing signaling complex-bound proximal caspases after exposure to TRAIL. We observed increased levels of both pro- and antiapoptotic BCL-2 proteins at the mitochondria following exposure to roscovitine. These results suggest that roscovitine induces priming of cancer cells for death by binding antiapoptotic BCL-2 proteins to proapoptotic BH3-only proteins at the mitochondria, thereby decreasing the threshold for diverse proapoptotic stimuli. We propose that the mitochondrial priming and enhanced processing of apical caspases represent major molecular mechanisms of roscovitine-induced sensitization to TRAIL in leukemia/lymphoma cells.

• MeSH
• apoptóza účinky léků   MeSH
• cytotoxicita imunologická účinky léků   MeSH
• genetická transkripce účinky léků   MeSH
• leukemie genetika   metabolismus   patologie   MeSH
• lidé MeSH
• ligand Fas farmakologie   MeSH
• lymfom genetika   metabolismus   patologie   MeSH
• mitochondrie účinky léků   metabolismus   MeSH
• myši MeSH
• nádorové buněčné linie MeSH
• protein bcl-X metabolismus   MeSH
• protein MCL-1 MeSH
• protein TRAIL farmakologie   MeSH
• proteosyntéza účinky léků   MeSH
• protinádorové látky farmakologie   MeSH
• protoonkogenní proteiny c-bcl-2 metabolismus   MeSH
• puriny farmakologie   MeSH
• roskovitin MeSH
• signální adaptorové proteiny receptorové domény smrti metabolismus   MeSH
• TNF-alfa farmakologie   MeSH
• tumor burden účinky léků   MeSH
• xenogenní modely - testy protinádorové aktivity MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• ligand Fas MeSH
• protein bcl-X MeSH
• protein MCL-1 MeSH
• protein TRAIL MeSH
• protinádorové látky MeSH
• protoonkogenní proteiny c-bcl-2 MeSH
• puriny MeSH
• roskovitin MeSH
• signální adaptorové proteiny receptorové domény smrti MeSH
• TNF-alfa MeSH

Trichothecene mycotoxin deoxynivalenol (DON) negatively regulates immune response by damaging host immune system and harming the organism's health. We hypothesized that DON can initiate an active immunosuppressive mechanism similar to "immune evasion" to alter the cellular microenvironment and evade immune surveillance. We tested this hypothesis using the RAW264.7 macrophage model. DON rapidly increased the expression of immune checkpoints PD-1 and PD-L1, inflammatory cytokine TGF-β, and key immune evasion factors STAT3, VEGF, and TLR-4, and caused cellular hypoxia. Importantly, hypoxia-inducible factor-1α (HIF-1α) acts as a key regulator of DON-induced immunosuppression. HIF-1α accumulated in the cytoplasm and was gradually transferred to the nucleus following DON treatment. Moreover, DON activated HIF-1α through STAT3 signaling to upregulate downstream signaling, including PD-1/PD-L1. Under DON treatment, immunosuppressive miR-210-3p, lncRNA PVT1, lncRNA H19, and lncRNA HOTAIR were upregulated by the STAT3/HIF-1α axis. Moreover, DON damaged mitochondrial function, causing mitophagy, and suppressed immune defenses. Collectively, DON triggered RAW264.7 intracellular hypoxia and rapidly activated HIF-1α via STAT3 signaling, activating immune evasion signals, miRNAs, and lncRNAs, thereby initiating the key link of immune evasion. This study offers further clues for accurate prevention and treatment of immune diseases caused by mycotoxins.

• Klíčová slova
• Deoxynivalenol, HIF-1, Immune evasion, STAT3, lncRNA,
• MeSH
• antigeny CD274 * metabolismus   MeSH
• antigeny CD279 MeSH
• faktor 1 indukovatelný hypoxií - podjednotka alfa metabolismus   MeSH
• imunita MeSH
• nádorové buněčné linie MeSH
• RNA dlouhá nekódující * MeSH
• transkripční faktor STAT3 metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• antigeny CD274 * MeSH
• antigeny CD279 MeSH
• deoxynivalenol MeSH Prohlížeč
• faktor 1 indukovatelný hypoxií - podjednotka alfa MeSH
• RNA dlouhá nekódující * MeSH
• transkripční faktor STAT3 MeSH

The sesquiterpenoid juvenile hormone (JH) is vital to insect development and reproduction. Intracellular JH receptors have recently been established as basic helix-loop-helix transcription factor (bHLH)/PAS proteins in Drosophila melanogaster known as germ cell-expressed (Gce) and its duplicate paralog, methoprene-tolerant (Met). Upon binding JH, Gce/Met activates its target genes. Insects possess multiple native JH homologs whose molecular activities remain unexplored, and diverse synthetic compounds including insecticides exert JH-like effects. How the JH receptor recognizes its ligands is unknown. To determine which structural features define an active JH receptor agonist, we tested several native JHs and their nonnative geometric and optical isomers for the ability to bind the Drosophila JH receptor Gce, to induce Gce-dependent transcription, and to affect the development of the fly. Our results revealed high ligand stereoselectivity of the receptor. The geometry of the JH skeleton, dictated by two stereogenic double bonds, was the most critical feature followed by the presence of an epoxide moiety at a terminal position. The optical isomerism at carbon C11 proved less important even though Gce preferentially bound a natural JH enantiomer. The results of receptor-ligand-binding and cell-based gene activation assays tightly correlated with the ability of different geometric JH isomers to induce gene expression and morphogenetic effects in the developing insects. Molecular modeling supported the requirement for the proper double-bond geometry of JH, which appears to be its major selective mechanism. The strict stereoselectivity of Gce toward the natural hormone contrasts with the high potency of synthetic Gce agonists of disparate chemistries.

• Klíčová slova
• Drosophila, basic helix-loop-helix transcription factor (bHLH), development, hormone receptor, insect, juvenile hormone (JH), ligand-binding protein, reproduction, stereoselectivity,
• MeSH
• Drosophila melanogaster chemie   genetika   metabolismus   MeSH
• juvenilní hormony chemie   metabolismus   MeSH
• molekulární modely MeSH
• proteiny Drosophily metabolismus   MeSH
• receptory buněčného povrchu metabolismus   MeSH
• stereoizomerie MeSH
• transkripční faktory bHLH metabolismus   MeSH
• transkripční faktory metabolismus   MeSH
• vazba proteinů MeSH
• vývojová regulace genové exprese MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• gce protein, Drosophila MeSH Prohlížeč
• juvenilní hormony MeSH
• MET protein, Drosophila MeSH Prohlížeč
• proteiny Drosophily MeSH
• receptory buněčného povrchu MeSH
• transkripční faktory bHLH MeSH
• transkripční faktory MeSH

The effects of four copper(II) mixed-ligand complexes [Cu(qui1)(L)]NO3·H2O (1-3) and [Cu(qui2)(phen)]NO3 (4), where qui1=2-phenyl-3-hydroxy-4(1H)-quinolinone, Hqui2=2-(4-amino-3,5-dichlorophenyl)-N-propyl-3-hydroxy-4(1H)-quinolinone-7-carboxamide, L=1,10-phenanthroline (phen) (1), 5-methyl-1,10-phenanthroline (mphen) (2), bathophenanthroline (bphen) (3), on transcriptional activities of steroid receptors, nuclear receptors and xenoreceptors have been studied. The complexes (1-4) did not influence basal or ligand-inducible activities of glucocorticoid receptor, androgen receptor, thyroid receptor, pregnane X receptor and vitamin D receptor, as revealed by gene reporter assays. The complexes 1 and 2 dose-dependently induced luciferase activity in stable gene reporter AZ-AhR cell line, and this induction was reverted by resveratrol, indicating involvement of aryl hydrocarbon receptor (AhR) in the process. The complexes 1, 2 and 3 induced CYP1A1 mRNA in LS180 cells and CYP1A1/CYP1A2 in human hepatocytes through AhR. Electrophoretic mobility shift assay EMSA showed that the complexes 1 and 2 transformed AhR in its DNA-binding form. Collectively, we demonstrate that the complexes 1 and 2 activate AhR and induce AhR-dependent genes in human hepatocytes and cancer cell lines. In conclusion, the data presented here might be of toxicological importance, regarding the multiple roles of AhR in human physiology and pathophysiology.

• Klíčová slova
• Copper(II) complexes, Cytochrome P450, Human hepatocytes, Nuclear receptors, Xenobiotics,
• MeSH
• aktivace transkripce účinky léků   MeSH
• cytochrom P-450 CYP1A1 biosyntéza   genetika   MeSH
• cytochrom P-450 CYP1A2 biosyntéza   genetika   MeSH
• dospělí MeSH
• dusičnany toxicita   MeSH
• enzymová indukce MeSH
• fenantroliny toxicita   MeSH
• genetická transkripce účinky léků   MeSH
• hepatocyty účinky léků   enzymologie   MeSH
• lidé středního věku MeSH
• lidé MeSH
• ligandy MeSH
• měď toxicita   MeSH
• messenger RNA biosyntéza   genetika   MeSH
• MFC-7 buňky MeSH
• primární buněčná kultura MeSH
• receptory aromatických uhlovodíků agonisté   genetika   metabolismus   MeSH
• senioři MeSH
• transfekce MeSH
• transkripční faktory bHLH agonisté   genetika   metabolismus   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• 1,10-phenanthroline MeSH Prohlížeč
• AHR protein, human MeSH Prohlížeč
• copper(II) nitrate MeSH Prohlížeč
• CYP1A1 protein, human MeSH Prohlížeč
• CYP1A2 protein, human MeSH Prohlížeč
• cytochrom P-450 CYP1A1 MeSH
• cytochrom P-450 CYP1A2 MeSH
• dusičnany MeSH
• fenantroliny MeSH
• ligandy MeSH
• měď MeSH
• messenger RNA MeSH
• receptory aromatických uhlovodíků MeSH
• transkripční faktory bHLH MeSH

Important key players in the regulatory machinery within the cells are nuclear retinoid X receptors (RXRs), which compose heterodimers in company with several diverse nuclear receptors, playing a role as ligand inducible transcription factors. In general, nuclear receptors are ligand-activated, transcription-modulating proteins affecting transcriptional responses in target genes. RXR molecules forming permissive heterodimers with disparate nuclear receptors comprise peroxisome proliferator-activated receptors (PPARs), liver X receptors (LXRs), farnesoid X receptor (FXR), pregnane X receptor (PXR) and constitutive androstan receptor (CAR). Retinoid receptors (RARs) and thyroid hormone receptors (TRs) may form conditional heterodimers, and dihydroxyvitamin D3 receptor (VDR) is believed to form nonpermissive heterodimer. Thus, RXRs are the important molecules that are involved in control of many cellular functions in biological processes and diseases, including cancer or diabetes. This article summarizes both naturally occurring and synthetic ligands for nuclear retinoid X receptors and describes, predominantly in mammals, their role in molecular mechanisms within the cells. A focus is also on triorganotin compounds, which are high affinity RXR ligands, and finally, we present an outlook on human microbiota as a potential source of RXR activators. Nevertheless, new synthetic rexinoids with better retinoid X receptor activity and lesser side effects are highly required.

• Klíčová slova
• Human microbiota, Ligand inducible transcription factors, Natural and synthetic RXR ligands, Nuclear receptors, Retinoid X receptors (RXR),
• MeSH
• lidé MeSH
• ligandy MeSH
• mikrobiota MeSH
• organocínové sloučeniny farmakologie   MeSH
• receptory cytoplazmatické a nukleární fyziologie   MeSH
• retinoidní X receptory agonisté   fyziologie   MeSH
• tretinoin analogy a deriváty   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• ligandy MeSH
• organocínové sloučeniny MeSH
• receptory cytoplazmatické a nukleární MeSH
• retinoidní X receptory MeSH
• tretinoin MeSH

The efforts for therapeutic targeting of the aryl hydrocarbon receptor (AhR) have emerged in recent years. We investigated the effects of available antimigraine triptan drugs, having an indole core in their structure, on AhR signaling in human hepatic and intestinal cells. Activation of AhR in reporter gene assays was observed for Avitriptan and to a lesser extent for Donitriptan, while other triptans were very weak or no activators of AhR. Using competitive binding assay and by homology docking, we identified Avitriptan as a low-affinity ligand of AhR. Avitriptan triggered nuclear translocation of AhR and increased binding of AhR in CYP1A1 promotor DNA, as revealed by immune-fluorescence microscopy and chromatin immune-precipitation assay, respectively. Strong induction of CYP1A1 mRNA was achieved by Avitriptan in wild type but not in AhR-knockout, immortalized human hepatocytes, implying that induction of CYP1A1 is AhR-dependent. Increased levels of CYP1A1 mRNA by Avitriptan were observed in human colon carcinoma cells LS180 but not in primary cultures of human hepatocytes. Collectively, we show that Avitriptan is a weak ligand and activator of human AhR, which induces the expression of CYP1A1 in a cell-type specific manner. Our data warrant the potential off-label therapeutic application of Avitriptan as an AhR-agonist drug.

• Klíčová slova
• Antimigraine drugs, Aryl Hydrocarbon Receptor, Triptans, repurposing,
• MeSH
• aktivace enzymů účinky léků   MeSH
• cytochrom P-450 CYP1A1 genetika   MeSH
• hepatocyty metabolismus   MeSH
• kultivované buňky MeSH
• lidé MeSH
• ligandy MeSH
• molekulární modely MeSH
• orgánová specificita MeSH
• přehodnocení terapeutických indikací léčivého přípravku MeSH
• promotorové oblasti (genetika) účinky léků   MeSH
• receptory aromatických uhlovodíků agonisté   chemie   metabolismus   MeSH
• simulace molekulového dockingu MeSH
• střevní sliznice metabolismus   MeSH
• sulfonamidy farmakologie   MeSH
• transkripční faktory bHLH agonisté   chemie   metabolismus   MeSH
• tryptaminy farmakologie   MeSH
• upregulace MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• AHR protein, human MeSH Prohlížeč
• avitriptan MeSH Prohlížeč
• CYP1A1 protein, human MeSH Prohlížeč
• cytochrom P-450 CYP1A1 MeSH
• ligandy MeSH
• receptory aromatických uhlovodíků MeSH
• sulfonamidy MeSH
• transkripční faktory bHLH MeSH
• tryptaminy MeSH

A major outcome of the canonical Wnt/beta-catenin-signalling pathway is the transcriptional activation of a specific set of target genes. A typical feature of the transcriptional response induced by Wnt signalling is the involvement of Tcf/Lef factors that function in the nucleus as the principal mediators of signalling. Vertebrate Tcf/Lef proteins perform two well-characterized functions: in association with beta-catenin they activate gene expression, and in the absence of Wnt ligands they bind TLE/Groucho proteins to act as transcriptional repressors. Although the general characteristics of Tcf/Lef factors are well understood, the mechanisms that control their specific roles in various cellular backgrounds are much less defined. In this report we reveal that the evolutionary conserved Dazap2 protein functions as a TCF-4 interacting partner. We demonstrate that a short region proximal to the TCF-4 HMG box mediates the interaction and that all Tcf/Lef family members associate with Dazap2. Interestingly, knockdown of Dazap2 not only reduced the activity of Wnt signalling as measured by Tcf/beta-catenin reporters but additionally altered the expression of Wnt-signalling target genes. Finally, chromatin immunoprecipitation studies indicate that Dazap2 modulates the affinity of TCF-4 for its DNA-recognition motif.

• MeSH
• beta-katenin metabolismus   MeSH
• buněčné linie MeSH
• DNA vazebné proteiny chemie   metabolismus   MeSH
• genetická transkripce * MeSH
• genový knockdown MeSH
• lidé MeSH
• myši MeSH
• promotorové oblasti (genetika) MeSH
• proteiny vázající RNA antagonisté a inhibitory   genetika   metabolismus   MeSH
• proteiny Wnt metabolismus   MeSH
• regulace genové exprese MeSH
• transkripční faktor 4 MeSH
• transkripční faktory BHLH-Zip MeSH
• transkripční faktory chemie   metabolismus   MeSH
• vazebná místa MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• beta-katenin MeSH
• DAZAP2 protein, human MeSH Prohlížeč
• DNA vazebné proteiny MeSH
• proteiny vázající RNA MeSH
• proteiny Wnt MeSH
• TCF4 protein, human MeSH Prohlížeč
• transkripční faktor 4 MeSH
• transkripční faktory BHLH-Zip MeSH
• transkripční faktory MeSH

Fas ligand (FasL, CD178) belongs to classical apoptotic molecules, however, recent evidence expands the spectrum of FasL functions into non-apoptotic processes which also applies for the bone. Tgfb subfamily members (Tgfb1, Tgfb2, Tgfb3) represent major components in osteogenic pathways and extracellular matrix. Their possible association with FasL has not yet been investigated but can be postulated. To test such a hypothesis, FasL deficient (gld) calvaria-derived cells were examined with a focus on the expression of Tgfb receptor ligands. The qPCR analysis revealed significantly increased expression of Tgfb1, Tgfb2 and Tgfb3 in gld cells. To check the vice versa effect, the gld cells were stimulated by soluble FasL. As a consequence, a dramatic decrease in expression levels of all three ligands was observed. This phenomenon was also confirmed in IDG-SW3 (osteoblastic cells of endochondral origin). TFLink gateway identified Fosl2 as an exclusive candidate of FasL capable to impact expression of all three Tgfb ligands. However, Fosl2 siRNA did not cause any significant changes in expression of Tgfb ligands. Therefore, the upregulation of the three ligands is likely to occur separately. In this respect, we tested the only exclusive candidate transcription factor for Tgfb3, Prrx1. Additionally, an overlapping candidate for Tgfb1 and Tgfb2, Mef2c capable to modulate expression of sclerostin, was examined. Prrx1 as well as Mef2c were found upregulated in gld samples and their expression decreased after addition of FasL. The same effect of FasL treatment was observed in the IDG-SW3 model. Taken together, FasL deficiency causes an increase in the expression of Tgfb ligands and stimulation by FasL reduces Tgfb expression in osteoblastic cells. The candidates mediating the effect comprise Prrx1 for Tgfb3 and Mef2c for Tgfb1/2. These results indicate FasL as a novel cytokine interfering with Tgfb signaling and thus the complex osteogenic network. The emerging non-apoptotic functions of FasL in bone development and maintenance should also be considered in treatment strategies such as the anti-osteoporotic factor.

• Klíčová slova
• ECM, Fas ligand, Fosl2, Mef2c, Prrx1, Tgfb,
• MeSH
• buněčné linie MeSH
• ligand Fas * metabolismus   MeSH
• myši MeSH
• osteoblasty * metabolismus   MeSH
• signální transdukce * MeSH
• transformující růstový faktor beta metabolismus   MeSH
• transformující růstový faktor beta1 metabolismus   farmakologie   MeSH
• transformující růstový faktor beta2 metabolismus   farmakologie   MeSH
• transformující růstový faktor beta3 * metabolismus   genetika   MeSH
• transkripční faktory MEF2 metabolismus   genetika   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• ligand Fas * MeSH
• Mef2c protein, mouse MeSH Prohlížeč
• transformující růstový faktor beta MeSH
• transformující růstový faktor beta1 MeSH
• transformující růstový faktor beta2 MeSH
• transformující růstový faktor beta3 * MeSH
• transkripční faktory MEF2 MeSH