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Artykuły w czasopismach na temat „Rottlerin”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Lee, Bogyeong, Jeongho Jeong, Hyun Kyung Kim, et al. "Rottlerin Promotes Beigeing and Non-Shivering Thermogenesis via LRP6 Inhibition." Food Engineering Progress 28, no. 2 (2024): 93–102. http://dx.doi.org/10.13050/foodengprog.2024.28.2.93.

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Obesity, characterized by excessive fat accumulation, poses global health risks, including metabolic disorders like type 2 diabetes and cardiovascular diseases, with its prevalence steadily rising. This study proposes that rottlerin induces anti-obesity effects by enhancing non-shivering thermogenesis in beige adipocytes D16 via LRP6 inhibition. As a result, treatment of D16 cells with rottlerin up to 5 μM showed no cytotoxicity. Rottlerin significantly increased the expression of proteins involved in substrate oxidation, such as UCP1 and PGC1α, while decreasing the expression of C/EBPβ associ

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Chen, Xu‐Ling, Yu Dong, and Ji‐Yu Wang. "The Practical Total Synthesis of Rottlerin and Rottlerone." ChemistrySelect 5, no. 29 (2020): 9206–9. http://dx.doi.org/10.1002/slct.202002245.

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Kim, Hyun Kyung, Eun Young Kang, and Gwang-woong Go. "Rottlerin, a Polyphenolic Compound, Alleviate Body Adiposity by Enhancing Lipolysis and Thermogenesis in Diet-Induced Obesity Mice." Current Developments in Nutrition 5, Supplement_2 (2021): 1222. http://dx.doi.org/10.1093/cdn/nzab055_032.

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Abstract Objectives Rottlerin (mallotoxin) is a polyphenolic compound in Mallotus philippensis. The anti-tumor, anti-inflammation, and mitochondrial uncoupling regulation effects of rottlerin have been known. However, the anti-obesity effect was not reported yet. Thus, we hypothesized that rottlerin would suppress body fat accumulation in obesity-induced mice. Methods Five-week-old male C57BL/6 mice were fed a high-fat diet (HFD) (60% kcal from fat) ad libitum for 8 weeks. Mice were randomly assigned to five groups as follows: 1) normal diet (18% kcal from fat), 2) negative control (60% kcal f

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4

Shivshankar, Pooja, Lei Lei, Jie Wang, and Guangming Zhong. "Rottlerin Inhibits Chlamydial Intracellular Growth and Blocks Chlamydial Acquisition of Sphingolipids from Host Cells." Applied and Environmental Microbiology 74, no. 4 (2007): 1243–49. http://dx.doi.org/10.1128/aem.02151-07.

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ABSTRACT We report that rottlerin, a plant-derived compound known to inhibit various mammalian kinases, profoundly inhibited chlamydial growth in cell culture with a minimal inhibition concentration of 1 μM. The inhibition was effective even when rottlerin was added as late as the middle stage of chlamydial infection cycle, against multiple Chlamydia species, and in different host cell lines. Pretreatment of host cells with rottlerin prior to infection also blocked chlamydial growth, suggesting that rottlerin targets host factors. Moreover, rottlerin did not alter the chlamydial infection rate

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Kim, Ye Jin, and Gwang-woong !Go. "Rottlerin Suppresses Fat Accumulation by Inhibiting Adipogenesis and De Novo Lipogenesis in 3T3-L1 Adipocytes." Current Developments in Nutrition 5, Supplement_2 (2021): 1224. http://dx.doi.org/10.1093/cdn/nzab055_034.

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Abstract Objectives Rottlerin is isolated from Mallotus japonicus, a rich-in polyphenol. Rottlerin is a PKC delta inhibitor known for an uncoupler of oxidative phosphorylation and anti-neoplastic agent. However, the effect of anti-obesity is not conclusive. This study hypothesized that rottlerin inhibits lipid accumulation in adipocytes. Methods 3T3-L1 cells were maintained with DMEM containing 10% BCS and 1% penicillin. The cells were seeded in a 6-well plate with a density of 8 × 104 followed by cultured for 4 days until reaching 120% confluency and incubated in a differentiation medium for

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6

Ohno, Izumi, Guido Eibl, Irina Odinokova, et al. "Rottlerin stimulates apoptosis in pancreatic cancer cells through interactions with proteins of the Bcl-2 family." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 1 (2010): G63—G73. http://dx.doi.org/10.1152/ajpgi.00257.2009.

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Rottlerin is a polyphenolic compound derived from Mallotus philipinensis . In the present study, we show that rottlerin decreased tumor size and stimulated apoptosis in an orthotopic model of pancreatic cancer with no effect on normal tissues in vivo. Rottlerin also induced apoptosis in pancreatic cancer (PaCa) cell lines by interacting with mitochondria and stimulating cytochrome c release. Immunoprecipitation results indicated that rottlerin disrupts complexes of prosurvival Bcl-xL with Bim and Puma. Furthermore, siRNA knockdown showed that Bim and Puma are necessary for rottlerin to stimula

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7

Kim, Younhee, Jeongho Jeong, Sumin Kang та ін. "Rottlerin Inhibits Lipid Accumulation in Differentiated 3T3-L1 Cells through LRP6/β-Catenin/TCF7L2 Down-Regulation". Food Engineering Progress 28, № 3 (2024): 225–33. http://dx.doi.org/10.13050/foodengprog.2024.28.3.225.

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Obesity, a global health concern characterized by excessive fat accumulation, necessitates the discovery of anti-obesity compounds. Rottlerin, known for its anti-cancer effects as a mitochondrial uncoupler, has been a subject of interest. However, its impact on reducing intracellular lipid accumulation remains a gap in our understanding. This study aimed to fill this gap by dissecting the mechanism of rottlerin in 3T3-L1 adipocytes. We treated differentiated 3T3-L1 cells with 0-20 μM of rottlerin for 48 hours to assess its capability to induce lipid accumulation. Notably, we observed no cytoto

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8

Maioli, Emanuela, Lucedio Greci, Karel Soucek та ін. "Rottlerin Inhibits ROS Formation and Prevents NFκB Activation in MCF-7 and HT-29 Cells". Journal of Biomedicine and Biotechnology 2009 (2009): 1–7. http://dx.doi.org/10.1155/2009/742936.

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Rottlerin, a polyphenol isolated from Mallotus Philippinensis, has been recently used as a selective inhibitor of PKCδ, although it can inhibit many kinases and has several biological effects. Among them, we recently found that Rottlerin inhibits the Nuclear FactorκB (NFκB), activated by either phorbol esters orH2O2. Because of the redox sensitivity of NFκB and on the basis of Rottlerin antioxidant property, we hypothesized that Rottlerin could prevent NFκB activation acting as a free radicals scavenger, as other natural polyphenols. The current study confirms the antioxidant property of Rottl

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9

Molina, Yessenia L., David García-Seisdedos, Bohdan Babiy, et al. "Rottlerin Stimulates Exosome/Microvesicle Release Via the Increase of Ceramide Levels Mediated by Ampk in an In Vitro Model of Intracellular Lipid Accumulation." Biomedicines 10, no. 6 (2022): 1316. http://dx.doi.org/10.3390/biomedicines10061316.

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Exosomes/microvesicles originate from multivesicular bodies that allow the secretion of endolysosome components out of the cell. In the present work, we investigated the effects of rottlerin, a polyphenol, on exosome/microvesicle secretion in a model of intracellular lipid trafficking impairment, and elucidated the mechanism of action. In a model of lipid trafficking impairment in C6 glia cells, rottlerin increased ceramide levels, while decreasing hexosylceramide content. This was accompanied by increased exosome/microvesicle secretion, thereby reducing the concentration of lipids in the endo

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10

Kang, Yeonglim, Jong-Chul Choi, Joong-Bok Lee, Seung-Yong Park та Changin Oh. "Rottlerin inhibits macropinocytosis of Porcine Reproductive and Respiratory Syndrome Virus through the PKCδ-Cofilin signaling pathway". PLOS One 20, № 5 (2025): e0324500. https://doi.org/10.1371/journal.pone.0324500.

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Rottlerin exerts antiviral activity against various enveloped viruses, yet the mechanism by which it inhibits viral replication and the associated signaling pathways remains unclear. Here, we investigated the mechanisms for the antiviral effects of rottlerin against Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) in vitro. We demonstrate that PRRSV enters host cells via macropinocytosis. Rottlerin, a PKCδ inhibitor, partially inhibits PRRSV entry by decreasing actin polymerization, as evidenced by alterations in actin dynamics. LIM domain kinase 1 (LIMK1) is essential for PRRSV rep

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11

Mischitelli, Morena, Mohamed Jemaà, Mustafa Almasry, Caterina Faggio, and Florian Lang. "Stimulation of Suicidal Erythrocyte Death by Rottlerin." Cellular Physiology and Biochemistry 40, no. 3-4 (2016): 558–66. http://dx.doi.org/10.1159/000452569.

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Background/Aims: The phytochemical polyphenol rottlerin is a potent activator of diverse Ca2+ -sensitive K+ channels. Those channels play a decisive role in the execution of eryptosis, the suicidal death of erythrocytes, which is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling involved in the stimulation of eryptosis includes increase of cytosolic Ca2+ activity ([Ca2+]i) and ceramide. The present study explored, whether rottlerin induces eryptosis and, if so, to test for the involvement of Ca2+ entry and c

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12

Matschke, Veronika, Ilaria Piccini, Janina Schubert, et al. "The Natural Plant Product Rottlerin Activates Kv7.1/KCNE1 Channels." Cellular Physiology and Biochemistry 40, no. 6 (2016): 1549–58. http://dx.doi.org/10.1159/000453205.

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Background/Aims: Acquired as well as inherited channelopathies are disorders that are caused by altered ion channel function. A family of channels whose malfunction is associated with different channelopathies is the Kv7 K+ channel family; and restoration of normal Kv7 channel function by small molecule modulators is a promising approach for treatment of these often fatal diseases. Methods: Here, we show the modulation of Kv7 channels by the natural compound Rottlerin heterologously expressed in Xenopus laevis oocytes and on iPSC cardiomyocytes overexpressing Kv7.1 channels. Results: We show t

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13

Klinger, James R., Josh D. Murray, Brian Casserly та ін. "Rottlerin causes pulmonary edema in vivo: a possible role for PKCδ". Journal of Applied Physiology 103, № 6 (2007): 2084–94. http://dx.doi.org/10.1152/japplphysiol.00695.2007.

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In the present study, we assessed the effects of chemical inhibitors shown to be selective for protein kinase C (PKC) isoforms on lung barrier function both in vitro and in vivo. Rottlerin, a purported inhibitor of PKCδ, but not other chemical inhibitors, dose dependently promoted barrier dysfunction in lung endothelial cells in vitro. This barrier dysfunction correlated with structural changes in focal adhesions and stress fibers, which were consistent with functional changes in cell stiffness. To determine whether the effects noted in vitro correlated with changes in intact lungs, we tested

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14

Brown, Jared M., Corbin M. Schwanke, Mark A. Pershouse, Jean C. Pfau, and Andrij Holian. "Effects of rottlerin on silica-exacerbated systemic autoimmune disease in New Zealand mixed mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 6 (2005): L990—L998. http://dx.doi.org/10.1152/ajplung.00078.2005.

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Environmental crystalline silica exposure has been associated with formation of autoantibodies and development of systemic autoimmune disease, but the mechanisms leading to these events are unknown. Silica exposure in autoimmune-prone New Zealand mixed (NZM) mice results in a significant exacerbation of systemic autoimmunity as measured by increases in autoantibodies and glomerulonephritis. Previous studies have suggested that silica-induced apoptosis of alveolar macrophages (AM) contributes to the generation of the autoantibodies and disease. Rottlerin has been reported to inhibit apoptosis i

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Cordeiro, Brenda, Dmitry Terentyev, and Richard T. Clements. "BKCa channel activation increases cardiac contractile recovery following hypothermic ischemia/reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 4 (2015): H625—H633. http://dx.doi.org/10.1152/ajpheart.00818.2014.

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Mitochondrial Ca2+-activated large-conductance K+ (BKCa) channels are thought to provide protection during ischemic insults in the heart. Rottlerin (mallotoxin) has been implicated as a potent BKCa activator. The purpose of this study was twofold: 1) to investigate the efficacy of BKCa channel activation as a cardioprotective strategy during ischemic cardioplegic arrest and reperfusion (CP/R) and 2) to assess the specificity of rottlerin for BKCa channels. Wild-type (WT) and BKCa knockout (KO) mice were subjected to an isolated heart model of ischemic CP/R. A mechanism of rottlerin-induced car

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Zhao, Hongyu, Wei Tian та David M. Cohen. "Rottlerin inhibits tonicity-dependent expression and action of TonEBP in a PKCδ-independent fashion". American Journal of Physiology-Renal Physiology 282, № 4 (2002): F710—F717. http://dx.doi.org/10.1152/ajprenal.00303.2001.

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Novel protein kinase C (PKC) isoforms PKCδ and PKCε have recently been implicated in signaling by hypertonic stress. We investigated the role of the putative PKCδ inhibitor rottlerin on tonicity-dependent gene regulation. In the renal medullary mIMCD3 cell line, rottlerin blocked tonicity-dependent transcription of a tonicity enhancer (TonE)-driven luciferase reporter gene, as well as tonicity-dependent transcription of the physiological tonicity effector gene aldose reductase, but not urea-dependent transcription. Consistent with these data, rottlerin inhibited tonicity-dependent expression o

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Mody, Vandana D., Sivadasan Mangalan, Kalpesh K. Pandya, Ramanbhai B. Patel, and Balakrishna K. Chakravarthy. "Absorption of Herbinol—A Polyherbal Topical Cream." Journal of Pharmacy Technology 10, no. 2 (1994): 71–74. http://dx.doi.org/10.1177/875512259401000207.

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Objective: To determine serum absorption concentrations of two bioactive chemical markers (munjistin and rottlerin) of Herbinol, a topical polyherbal antiseptic cream. Design: Topical application of Herbinol cream on the back of albino rats on hair-free skin. Study: Serum concentrations of munjistin and rottlerin were estimated after application of Herbinol on the backs of the rats at 0,1, 2,3,4, and 24 hours and concentrations were quantified by high-performance-thin-layer chromatography. The validity of the procedure was verified by recovery studies by adding a known concentration of standar

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Ringshausen, Ingo, Kathrin Weick, Madlene Oelsner, Christian Peschel, and Thomas Decker. "Inhibition of Protein Kinase C (PKC) delta with Rottlerin Induces Apoptosis in B-CLL Cells, Augments Chemotherapeutic Cytotoxicity and Inhibits Antiapoptotic Survival Signals." Blood 104, no. 11 (2004): 2800. http://dx.doi.org/10.1182/blood.v104.11.2800.2800.

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Abstract Purpose: We have previously shown that PKC delta is constitutively activated in B-CLL cells. In the present study, we have analyzed the mechanism of apotosis induction as well as the effets of PKC delta in the presence of survival signal and chemotherapeutic agents. Methods: The mitochondrial membrane potential, presence of active caspase 3, conformational status of Bax and apoptosis assays (Annexin V stain, Tunel assay) were performed using flow cytometric analysis. Expression of BCL-2 family proteins and XIAP as well as processing of caspase 8 and 9 was revealed in western blot expe

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Daveri, Elena, Giuseppe Valacchi, Roberta Romagnoli, Emilia Maellaro, and Emanuela Maioli. "Antiproliferative Effect of Rottlerin on Sk-Mel-28 Melanoma Cells." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/545838.

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Melanoma is the most aggressive and chemoresistant form of skin cancer. Mutated, constitutively active B-RAF is believed to play a crucial role, although the selective B-RAF inhibition has shown poor clinical success, since phenomena of resistance usually occur, likely arising from additional genetic aberrations, such as loss of function of p53 and PTEN, overexpression of cyclin D1, hyperactivation of NF-κB, and downregulation of p21/Cip1. Since all of them are present in the Sk-Mel-28 melanoma cells, this cell line could be an ideal, albeit hard to study, model to develop new therapeutic stra

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Hong, Kenneth K. C., Graham E. Ball, David StC Black, and Naresh Kumar. "The Mosaic of Rottlerin." Journal of Organic Chemistry 80, no. 21 (2015): 10668–74. http://dx.doi.org/10.1021/acs.joc.5b01827.

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Suresh, Dittu, Shekh Sabir, Tsz Tin Yu, et al. "Natural Product Rottlerin Derivatives Targeting Quorum Sensing." Molecules 26, no. 12 (2021): 3745. http://dx.doi.org/10.3390/molecules26123745.

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Rottlerin is a natural product consisting of chalcone and flavonoid scaffolds, both of which have previously shown quorum sensing (QS) inhibition in various bacteria. Therefore, the unique rottlerin scaffold highlights great potential in inhibiting the QS system of Pseudomonas aeruginosa. Rottlerin analogues were synthesised by modifications at its chalcone- and methylene-bridged acetophenone moieties. The synthesis of analogues was achieved using an established five-step synthetic strategy for chalcone derivatives and utilising the Mannich reaction at C6 of the chromene to construct morpholin

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You, Bang-Jau, Yang-Chang Wu, Bo-Ying Bao, et al. "Rottlerin InhibitsLonicera japonica-Induced Photokilling in Human Lung Cancer Cells through Cytoskeleton-Related Signaling Cascade." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/193842.

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This study demonstrated that many apoptotic signaling pathways, such as Rho family, PKC family, MAP kinase family, and mitochondria-mediated apoptotic pathway, were triggered byLonicera japonicaextracts and irradiation in CH27 cells. Rottlerin, a PKCδ-selective inhibitor, reversed the photoactivatedLonicera japonicaextract-induced decrease in PKCδprotein expression and change in cell morphology in this study. In addition, rottlerin inhibited the photoactivatedLonicera japonica-induced decrease in protein expression of Ras, ERK, p38, PKCα, and PKCε, which are the kinases of prosurvival signalin

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Choi, Jong-Chul, Sung-Won Jung, In-Yeong Choi, et al. "Rottlerin-Liposome Inhibits the Endocytosis of Feline Coronavirus Infection." Veterinary Sciences 10, no. 6 (2023): 380. http://dx.doi.org/10.3390/vetsci10060380.

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Rottlerin (R) is a natural extract from Mallotus philippensis with antiviral properties. Feline infectious peritonitis (FIP) is a fatal disease caused by feline coronavirus (FCoV) that is characterized by systemic granulomatous inflammation and high mortality. We investigated the antiviral effect of liposome-loaded R, i.e., rottlerin-liposome (RL), against FCoV. We demonstrated that RL inhibited FCoV replication in a dose-dependent manner, not only in the early endocytosis stage but also in the late stage of replication. RL resolved the low solubility issue of rottlerin and improved its inhibi

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Maioli, E., C. Torricelli, and G. Valacchi. "Rottlerin and Cancer: Novel Evidence and Mechanisms." Scientific World Journal 2012 (2012): 1–11. http://dx.doi.org/10.1100/2012/350826.

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Because cancers are caused by deregulation of hundreds of genes, an ideal anticancer agent should target multiple gene products or signaling pathways simultaneously. Recently, extensive research has addressed the chemotherapeutic potential of plant-derived compounds. Among the ever-increasing list of naturally occurring anticancer agents, Rottlerin appears to have great potentiality for being used in chemotherapy because it affects several cell machineries involved in survival, apoptosis, autophagy, and invasion. The underlying mechanisms that have been described are diverse, and the final, ce

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Uecker, Marina, Rafaela da Silva, Thomas Grampp, Thomas Pasch, Marcus C. Schaub, and Michael Zaugg. "Translocation of Protein Kinase C Isoforms to Subcellular Targets in Ischemic and Anesthetic Preconditioning." Anesthesiology 99, no. 1 (2003): 138–47. http://dx.doi.org/10.1097/00000542-200307000-00023.

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Background Translocation of protein kinase C (PKC) to subcellular targets is a pivotal signaling step in ischemic preconditioning (IPC). However, to date, it is unknown whether PKC isoforms translocate in anesthetic preconditioning (APC). Methods The PKC blockers chelerythrine and rottlerin and the adenosine triphosphate-dependent potassium (K(ATP)) channel blockers HMR-1098 and 5-hydroxydecanoate were used to assess the role of PKC and K(ATP) channels in isolated perfused rat hearts subjected to IPC or APC (1.5 minimum alveolar concentration isoflurane) followed by 40 min of ischemia and 30 m

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Maioli, E., E. Daveri, E. Maellaro, F. Ietta, L. Cresti, and G. Valacchi. "Non-conventional rottlerin anticancer properties." Archives of Biochemistry and Biophysics 645 (May 2018): 50–53. http://dx.doi.org/10.1016/j.abb.2018.03.009.

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Torricelli, Claudia, Sara Salvadori, Giuseppe Valacchi, et al. "Alternative Pathways of Cancer Cell Death by Rottlerin: Apoptosis versus Autophagy." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/980658.

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Since the ability of cancer cells to evade apoptosis often limits the efficacy of radiotherapy and chemotherapy, autophagy is emerging as an alternative target to promote cell death. Therefore, we wondered whether Rottlerin, a natural polyphenolic compound with antiproliferative effects in several cell types, can induce cell death in MCF-7 breast cancer cells. The MCF-7 cell line is a good model of chemo/radio resistance, being both apoptosis and autophagy resistant, due to deletion of caspase 3 gene, high expression of the antiapoptotic protein Bcl-2, and low expression of the autophagic Becl

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Bahlis, Nizar J., Maya Starovic, Koen Raedschelders, Kathy Gratton, Oliver Bathe та Andrew Belch. "PKC δ Inhibition Restores PTEN Activity in Myeloma Cells and Prolongs Survival of GFP+ Myeloma SCID/NOD Mice In Vivo." Blood 106, № 11 (2005): 113. http://dx.doi.org/10.1182/blood.v106.11.113.113.

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Abstract PTEN, a cellular phosphatase involved in the regulation of phosphatidylinositol phosphates (PIPs), is often inactivated in myeloma cells either through gene mutation or via phosphorylation of serine and threonine residues in the PTEN C-terminal domain that also results in loss of its activity and stability. The loss of PTEN function results in a failure to de-phosphorylate PIPs with a corresponding increase in Akt kinase activity. We have recently reported that PKCδ inhibition with Rottlerin (3 μM) induces cell death in sensitive and resistant myeloma cell lines (MM1S, MM1R, 8226S and

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Qomaladewi, Nurinanda Prisky, Mi-Yeon Kim, and Jae Youl Cho. "Rottlerin Reduces cAMP/CREB-Mediated Melanogenesis via Regulation of Autophagy." International Journal of Molecular Sciences 20, no. 9 (2019): 2081. http://dx.doi.org/10.3390/ijms20092081.

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Melanogenesis is the sequential process of melanin production by melanocytes in order to protect the skin from harmful stimuli. Melanogenesis is disrupted by radiation exposure, which results in the differentiation of melanocytes into melanoma. Recently, some methods have been developed to maintain the instability of melanogenesis in melanoma by activating cellular autophagy. However, there is still a lack of knowledge about how autophagy is involved in the regulation of melanogenesis in melanoma cells. Here, we used rottlerin as an autophagy inducer to investigate the role of the cyclic adeno

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Guo, Benchang, Derek Blair, Thomas Chiles, Clifford Lowell, and Thomas Rothstein. "B Cell Receptor Crosstalk: The IL-4-induced Alternate Pathway for BCR Signaling Operates in Parallel with the Classical Pathway, Is Sensitive to Rottlerin, and Depends on Lyn (86.14)." Journal of Immunology 178, no. 1_Supplement (2007): S126. http://dx.doi.org/10.4049/jimmunol.178.supp.86.14.

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Abstract B cell exposure to IL-4 alters subsequent B cell receptor signaling such that ERK phosphorylation becomes signalosome-independent; however, the nature of this new, alternate signaling pathway and its relationship to the classical, signalosome-dependent signaling pathway, are not known. Here we report that the alternate and classical pathways for BCR signaling are differentially affected by rottlerin, and by Go6976 or LY294002, respectively. Further, in B cells lacking PKCâ, the classical pathway for BCR signaling is blocked, whereas the alternate pathway is little affected. Conversel

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De Witt, Bracken J., Alan D. Kaye, Ikhlass N. Ibrahim, et al. "Effects of PKC isozyme inhibitors on constrictor responses in the feline pulmonary vascular bed." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 1 (2001): L50—L57. http://dx.doi.org/10.1152/ajplung.2001.280.1.l50.

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The effects of Gö-6976, a Ca2+-dependent protein kinase C (PKC) isozyme inhibitor, and rottlerin, a PKC-δ isozyme/calmodulin (CaM)-dependent kinase III inhibitor, on responses to vasopressor agents were investigated in the feline pulmonary vascular bed. Injections of angiotensin II, norepinephrine (NE), serotonin, BAY K 8644, and U-46619 into the lobar arterial constant blood flow perfusion circuit caused increases in pressure. Gö-6976 reduced responses to angiotensin II; however, it did not alter responses to serotonin, NE, or U-46619, whereas Gö-6976 enhanced BAY K 8644 responses. Rottlerin

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Hong, Kenneth K. C., Kitty K. K. Ho, Mohan Bhadbhade, Graham E. Ball, David StC Black, and Naresh Kumar. "The Mosaic of Rottlerin: The Sequel." Journal of Natural Products 82, no. 5 (2019): 1190–99. http://dx.doi.org/10.1021/acs.jnatprod.8b00917.

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Valacchi, Giuseppe, Alessandra Pecorelli, Claudia Sticozzi, et al. "Rottlerin Exhibits Antiangiogenic Effects In vitro." Chemical Biology & Drug Design 77, no. 6 (2011): 460–70. http://dx.doi.org/10.1111/j.1747-0285.2011.01121.x.

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Maioli, Emanuela, Claudia Torricelli, and Giuseppe Valacchi. "Rottlerin and curcumin: a comparative analysis." Annals of the New York Academy of Sciences 1259, no. 1 (2012): 65–76. http://dx.doi.org/10.1111/j.1749-6632.2012.06514.x.

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Springael, Cécile, Séverine Thomas, Souad Rahmouni, et al. "Rottlerin inhibits human T cell responses." Biochemical Pharmacology 73, no. 4 (2007): 515–25. http://dx.doi.org/10.1016/j.bcp.2006.10.034.

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Gschwendt, M., H. J. Muller, K. Kielbassa, et al. "Rottlerin, a Novel Protein Kinase Inhibitor." Biochemical and Biophysical Research Communications 199, no. 1 (1994): 93–98. http://dx.doi.org/10.1006/bbrc.1994.1199.

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Welters, HJ, SA Smith, M. Tadayyon, JH Scarpello, and NG Morgan. "Evidence that protein kinase Cdelta is not required for palmitate-induced cytotoxicity in BRIN-BD11 beta-cells." Journal of Molecular Endocrinology 32, no. 1 (2004): 227–35. http://dx.doi.org/10.1677/jme.0.0320227.

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Chronic exposure of pancreatic beta-cells to saturated fatty acids leads to loss of viability, an effect that has been implicated in the process of beta-cell 'lipotoxicity' associated with the progression of type 2 diabetes. The mechanisms involved are unknown but recent evidence has implicated the delta isoform of protein kinase C (PKCdelta) in mediating fatty acid toxicity. We have investigated this proposition in the clonal insulin-secreting cell line, BRIN-BD11. BRIN-BD11 cells were found to undergo apoptosis when exposed to palmitate and this response was attenuated by the purportedly sel

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Wang, Fang, Hui-min Liu, Michael G. Irwin та ін. "Role of protein kinase C β2 activation in TNF-α-induced human vascular endothelial cell apoptosis". Canadian Journal of Physiology and Pharmacology 87, № 3 (2009): 221–29. http://dx.doi.org/10.1139/y09-004.

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The circulatory inflammatory cytokine tumor necrosis factor alpha (TNF-α) is increased in pathologic conditions that initiate or exacerbate vascular endothelial injury, such as diabetes. Protein kinase C (PKC) has been shown to play a critical role in TNF-α-induced human endothelial cell apoptosis. However, the relative roles played by specific isoforms of PKC in TNF-α-induced human endothelial cell apoptosis have not been addressed. We investigated the effects of a selective PKCβ2 inhibitor (CGP53353) on TNF-α-induced apoptosis in human vascular endothelial cells (cell line ECV304) and on the

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Barbaric, Ivana, Mark Jones, David J. Harley, Paul J. Gokhale, and Peter W. Andrews. "High-Content Screening for Chemical Modulators of Embryonal Carcinoma Cell Differentiation and Survival." Journal of Biomolecular Screening 16, no. 6 (2011): 603–17. http://dx.doi.org/10.1177/1087057111406547.

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Disentangling the complex interactions that govern stem cell fate choices of self-renewal, differentiation, or death presents a formidable challenge. Image-based phenotype-driven screening meets this challenge by providing means for rapid testing of many small molecules simultaneously. Pluripotent embryonal carcinoma (EC) cells offer a convenient substitute for embryonic stem (ES) cells in such screens because they are simpler to maintain and control. The authors developed an image-based screening assay to identify compounds that affect survival or differentiation of the human EC stem cell lin

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Petr, J., E. Chmelíková, A. Dörflerová, M. Ješeta, and Z. Kuthanová. "Effects of protein kinase C on parthenogenetic activation of pig oocytes using calcium ionophore or nitric oxide-donor." Czech Journal of Animal Science 52, No. 12 (2008): 415–22. http://dx.doi.org/10.17221/2336-cjas.

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Porcine oocytes matured <I>in vitr</I>o were activated for parthenogenetic development using either calcium ionophore (50&mu;M for 10 min) or nitric oxide donor SNAP (2mM for 23.5 hours). Protein kinase C (PKC) inhibitors, bisindolylmaleimide I or rottlerin, are able to inhibit parthenogenetic activation induced by calcium ionophore. The rate of activated oocytes decreased from 69% to 2% (<I>P</I> < 0.05) under the effect of bisindolylmaleimide I at a concentration of 0 or 20nM, respectively. The activation rate decreased from 68% to 0% (<I>P</I> <

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Liedtke, Carole M., та Thomas Cole. "Antisense oligodeoxynucleotide to PKC-δ blocks α1-adrenergic activation of Na-K-2Cl cotransport". American Journal of Physiology-Cell Physiology 273, № 5 (1997): C1632—C1640. http://dx.doi.org/10.1152/ajpcell.1997.273.5.c1632.

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A role for protein kinase C (PKC)-δ and -ζ isotypes in α1-adrenergic regulation of human tracheal epithelial Na-K-2Cl cotransport was studied with the use of isotype-specific PKC inhibitors and antisense oligodeoxynucleotides to PKC-δ or -ζ mRNA. Rottlerin, a PKC-δ inhibitor, blocked 72% of basolateral-to-apical, bumetanide-sensitive36Cl flux in nystatin-permeabilized cell monolayers stimulated with methoxamine, an α1-adrenergic agonist, with a 50% inhibitory concentration of 2.3 μM. Methoxamine increased PKC activity in cytosol and a particulate fraction; the response was insensitive to PKC-α

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Wang, Zhong, Gen-hai Shen, Jia-ming Xie, Bin Li, and Quan-gen Gao. "Rottlerin upregulates DDX3 expression in hepatocellular carcinoma." Biochemical and Biophysical Research Communications 495, no. 1 (2018): 1503–9. http://dx.doi.org/10.1016/j.bbrc.2017.11.198.

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Xavier, Alcides Euzebio Tavares, Luciana Chain Veronez, Luís Fernando Peinado Nagano, et al. "Low PRKAB2 Expression Is Associated with Poor Outcomes in Pediatric Adrenocortical Tumors, and Treatment with Rottlerin Increases the PRKAB2 Level and Inhibits Tumorigenic Aspects in the NCI-H295R Adrenocortical Cancer Cell Line." Cancers 16, no. 6 (2024): 1094. http://dx.doi.org/10.3390/cancers16061094.

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Pediatric adrenocortical tumors (ACTs) are rare, highly heterogeneous neoplasms with limited therapeutic options, making the investigation of new targets with potential therapeutic or prognostic purposes urgent. The PRKAB2 gene produces one of the subunits of the AMP-activated protein kinase (AMPK) complex and has been associated with cancer. However, little is known about the role AMPK plays in ACTs. We have evaluated how PRKAB2 is associated with clinical and biological characteristics in 63 pediatric patients with ACTs and conducted in vitro studies on the human NCI-H295R ACC cell line. An

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Liedtke, Carole M., Robert Papay та Thomas S. Cole. "Modulation of Na-K-2Cl cotransport by intracellular Cl− and protein kinase C-δ in Calu-3 cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 282, № 5 (2002): L1151—L1159. http://dx.doi.org/10.1152/ajplung.00143.2001.

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In this study, we tested the hypothesis that intracellular Cl−(Cl[Formula: see text]) regulates the activity of protein kinase C (PKC)-δ and thus the activation of Na-K-Cl cotransport (NKCC1) in a Calu-3 cell line. The α1-adrenergic agonist methoxamine (MOX) and hypertonic sucrose increased Cl[Formula: see text] and increased or decreased intracellular volume, respectively, without changing Cl[Formula: see text] concentration ([Cl−]i). Titration of [Cl−]i from 20–140 mM in nystatin-permeabilized cell monolayers did not affect the baseline activity of PKC-δ, PKC-ζ, or rottlerin-sensitive NKCC1.

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He, Peng, Nan Shen, Gongming Gao та ін. "Periodic Mechanical Stress Activates PKCδ-Dependent EGFR Mitogenic Signals in Rat Chondrocytes via PI3K-Akt and ERK1/2". Cellular Physiology and Biochemistry 39, № 4 (2016): 1281–94. http://dx.doi.org/10.1159/000447833.

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Background/Aims: The present study aimed to analyze the mechanisms by which periodic mechanical stress is translated into biochemical signals, and to verify the important role of signaling molecules including phosphatidylinositol-3-kinase (PI3K)-Akt, protein kinase C (PKC), and epidermal growth factor receptor (EGFR) in chondrocyte proliferation. The effects of periodic mechanical stress on the mitogenesis of chondrocytes have been studied extensively in recent years. However, the mechanisms underlying the ability of chondrocytes to sense and respond to periodic mechanical stress need further

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Maioli, Emanuela, and Giuseppe Valacchi. "Rottlerin: Bases for a Possible Usage in Psoriasis." Current Drug Metabolism 11, no. 5 (2010): 425–30. http://dx.doi.org/10.2174/138920010791526097.

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Valacchi, Giuseppe, Alessandra Pecorelli, Marzia Mencarelli, et al. "Rottlerin: a multifaced regulator of keratinocyte cell cycle." Experimental Dermatology 18, no. 6 (2009): 516–21. http://dx.doi.org/10.1111/j.1600-0625.2008.00816.x.

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SOLTOFF, S. "Rottlerin: an inappropriate and ineffective inhibitor of PKCδ". Trends in Pharmacological Sciences 28, № 9 (2007): 453–58. http://dx.doi.org/10.1016/j.tips.2007.07.003.

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Li, Yangfeng, Biao Yu, and Renxiao Wang. "Efficient synthesis of rottlerin and its two subunits." Tetrahedron Letters 57, no. 17 (2016): 1856–59. http://dx.doi.org/10.1016/j.tetlet.2016.03.049.

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Dietrich, Cornelia, Nicolas Gumpert, Isabelle Heit, Monika Borchert-Stuhlträger, Franz Oesch, and Raimund Wieser. "Rottlerin Induces a Transformed Phenotype in Human Keratinocytes." Biochemical and Biophysical Research Communications 282, no. 2 (2001): 575–79. http://dx.doi.org/10.1006/bbrc.2001.4530.

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