Relevant bibliographies by topics / Paraptosi

Academic literature on the topic 'Paraptosi'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Paraptosi"

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Raimondi, Michela, Fabrizio Fontana, Monica Marzagalli, Matteo Audano, Giangiacomo Beretta, Patrizia Procacci, Patrizia Sartori, Nico Mitro, and Patrizia Limonta. "Ca2+ overload- and ROS-associated mitochondrial dysfunction contributes to δ-tocotrienol-mediated paraptosis in melanoma cells." Apoptosis 26, no. 5-6 (April 3, 2021): 277–92. http://dx.doi.org/10.1007/s10495-021-01668-y.

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Abstract Melanoma is an aggressive tumor with still poor therapy outcomes. δ-tocotrienol (δ-TT) is a vitamin E derivative displaying potent anti-cancer properties. Previously, we demonstrated that δ-TT triggers apoptosis in human melanoma cells. Here, we investigated whether it might also activate paraptosis, a non-canonical programmed cell death. In accordance with the main paraptotic features, δ-TT was shown to promote cytoplasmic vacuolization, associated with endoplasmic reticulum/mitochondrial dilation and protein synthesis, as well as MAPK activation in A375 and BLM cell lines. Moreover, treated cells exhibited a significant reduced expression of OXPHOS complex I and a marked decrease in oxygen consumption and mitochondrial membrane potential, culminating in decreased ATP synthesis and AMPK phosphorylation. This mitochondrial dysfunction resulted in ROS overproduction, found to be responsible for paraptosis induction. Additionally, δ-TT caused Ca2+ homeostasis disruption, with endoplasmic reticulum-derived ions accumulating in mitochondria and activating the paraptotic signaling. Interestingly, by using both IP3R and VDAC inhibitors, a close cause-effect relationship between mitochondrial Ca2+ overload and ROS generation was evidenced. Collectively, these results provide novel insights into δ-TT anti-melanoma activity, highlighting its ability to induce mitochondrial dysfunction-mediated paraptosis. Graphic Abstract δ-tocotrienol induces paraptotic cell death in human melanoma cells, causing endoplasmic reticulum dilation and mitochondrial swelling. These alterations induce an impairment of mitochondrial function, ROS production and calcium overload.
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Balachandran, Chandrasekar, Kenta Yokoi, Kana Naito, Jebiti Haribabu, Yuichi Tamura, Masakazu Umezawa, Koji Tsuchiya, Toshitada Yoshihara, Seiji Tobita, and Shin Aoki. "Cyclometalated Iridium(III) Complex–Cationic Peptide Hybrids Trigger Paraptosis in Cancer Cells via an Intracellular Ca2+ Overload from the Endoplasmic Reticulum and a Decrease in Mitochondrial Membrane Potential." Molecules 26, no. 22 (November 21, 2021): 7028. http://dx.doi.org/10.3390/molecules26227028.

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In our previous paper, we reported that amphiphilic Ir complex–peptide hybrids (IPHs) containing basic peptides such as KK(K)GG (K: lysine, G: glycine) (e.g., ASb-2) exhibited potent anticancer activity against Jurkat cells, with the dead cells showing a strong green emission. Our initial mechanistic studies of this cell death suggest that IPHs would bind to the calcium (Ca2+)–calmodulin (CaM) complex and induce an overload of intracellular Ca2+, resulting in the induction of non-apoptotic programmed cell death. In this work, we conduct a detailed mechanistic study of cell death induced by ASb-2, a typical example of IPHs, and describe how ASb-2 induces paraptotic programmed cell death in a manner similar to that of celastrol, a naturally occurring triterpenoid that is known to function as a paraptosis inducer in cancer cells. It is suggested that ASb-2 (50 µM) induces ER stress and decreases the mitochondrial membrane potential (ΔΨm), thus triggering intracellular signaling pathways and resulting in cytoplasmic vacuolization in Jurkat cells (which is a typical phenomenon of paraptosis), while the change in ΔΨm values is negligibly induced by celastrol and curcumin. Other experimental data imply that both ASb-2 and celastrol induce paraptotic cell death in Jurkat cells, but this induction occurs via different signaling pathways.
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Lee, A. Reum, Min Ji Seo, Jin Kim, Dong Min Lee, In Young Kim, Mi Jin Yoon, Hur Hoon, and Kyeong Sook Choi. "Lercanidipine Synergistically Enhances Bortezomib Cytotoxicity in Cancer Cells via Enhanced Endoplasmic Reticulum Stress and Mitochondrial Ca2+ Overload." International Journal of Molecular Sciences 20, no. 24 (December 4, 2019): 6112. http://dx.doi.org/10.3390/ijms20246112.

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The proteasome inhibitor (PI), bortezomib (Btz), is effective in treating multiple myeloma and mantle cell lymphoma, but not solid tumors. In this study, we show for the first time that lercanidipine (Ler), an antihypertensive drug, enhances the cytotoxicity of various PIs, including Btz, carfilzomib, and ixazomib, in many solid tumor cell lines by inducing paraptosis, which is accompanied by severe vacuolation derived from the endoplasmic reticulum (ER) and mitochondria. We found that Ler potentiates Btz-mediated ER stress and ER dilation, possibly due to misfolded protein accumulation, in MDA-MB 435S cells. In addition, the combination of Btz and Ler triggers mitochondrial Ca2+ overload, critically contributing to mitochondrial dilation and subsequent paraptotic events, including mitochondrial membrane potential loss and ER dilation. Taken together, our results suggest that a combined regimen of PI and Ler may effectively kill cancer cells via structural and functional perturbations of the ER and mitochondria.
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Qian, Xi-Feng, Jia-Hao Zhang, Yue-Xue Mai, Xin Yin, Yu-Bin Zheng, Zi-Yuan Yu, Guo-Dong Zhu, and Xu-Guang Guo. "A Novel Insight into Paraptosis-Related Classification and Signature in Lower-Grade Gliomas." International Journal of Genomics 2022 (November 14, 2022): 1–32. http://dx.doi.org/10.1155/2022/6465760.

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Lower-grade gliomas (LGG) are the most common intracranial malignancies that readily evolve to high-grade gliomas and increase drug resistance. Paraptosis is defined as a nonapoptotic form of programmed cell death, which is gradually focused on patients with gliomas to develop treatment options. However, the specific role of paraptosis in LGG and its correlation is still vague. In this study, we first establish the novel paraptosis-based prognostic model for LGG patients. The relevant data of LGG patients were acquired from The Cancer Genome Atlas database, and we found that LGG patients could be divided into three different clusters based on paraptosis via consensus cluster analysis. Through least absolute shrinkage and selection operator regression analysis and multivariate Cox regression analysis, 10-paraptosis-related gene (PRG) signatures (CDK4, TNK2, DSTYK, CDKN3, CCR4, CASP9, HSPA5, RGR, LPAR1, and PDCD6IP) were identified to separate LGG patients into high- and low-risk subgroups successfully. The Kaplan–Meier analysis and time-dependent receiver-operating characteristic showed that the performances of predicting overall survival (OS) were dramatically high. The parallel results were reappeared and verified by using the Chinese Glioma Genome Atlas and Gene Expression Omnibus databases. Independent prognostic analysis and nomogram construction implied that risk scores could be considered the independent factor to predict OS. Enrichment analysis indicated that immune-related biological processes were generally enriched, and different immune statuses were highly infiltrated in high-risk group. We also confirmed the potential relationship of 10-PRG signatures and drug sensitivity of Food and Drug Administration–approved drugs. In summary, our findings provide a novel knowledge of paraptosis status and crucial direction to further explore the role of PRG signatures in LGG.
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Nguyen, Phuong Linh, Chang Hoon Lee, Heesoon Lee, and Jungsook Cho. "Induction of Paraptotic Cell Death in Breast Cancer Cells by a Novel Pyrazolo[3,4-h]quinoline Derivative through ROS Production and Endoplasmic Reticulum Stress." Antioxidants 11, no. 1 (January 5, 2022): 117. http://dx.doi.org/10.3390/antiox11010117.

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Chemotherapy has been a standard intervention for a variety of cancers to impede tumor growth, mainly by inducing apoptosis. However, development of resistance to this regimen has led to a growing interest and demand for drugs targeting alternative cell death modes, such as paraptosis. Here, we designed and synthesized a novel derivative of a pyrazolo[3,4-h]quinoline scaffold (YRL1091), evaluated its cytotoxic effect, and elucidated the underlying molecular mechanisms of cell death in MDA-MB-231 and MCF-7 breast cancer (BC) cells. We found that YRL1091 induced cytotoxicity in these cells with numerous cytoplasmic vacuoles, one of the distinct characteristics of paraptosis. YRL1091-treated BC cells displayed several other distinguishing features of paraptosis, excluding autophagy or apoptosis. Briefly, YRL1091-induced cell death was associated with upregulation of microtubule-associated protein 1 light chain 3B, downregulation of multifunctional adapter protein Alix, and activation of extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase. Furthermore, the production of reactive oxygen species (ROS) and newly synthesized proteins were also observed, subsequently causing ubiquitinated protein accumulation and endoplasmic reticulum (ER) stress. Collectively, these results indicate that YRL1091 induces paraptosis in BC cells through ROS generation and ER stress. Therefore, YRL1091 can serve as a potential candidate for the development of a novel anticancer drug triggering paraptosis, which may provide benefit for the treatment of cancers resistant to conventional chemotherapy.
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Liu, Xiaoli, Yan Gu, Yaoyao Bian, Danhong Cai, Yu Li, Ye Zhao, Zhaofeng Zhang, Mei Xue, and Liang Zhang. "Honokiol induces paraptosis-like cell death of acute promyelocytic leukemia via mTOR & MAPK signaling pathways activation." Apoptosis 26, no. 3-4 (February 7, 2021): 195–208. http://dx.doi.org/10.1007/s10495-020-01655-9.

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AbstractAcute promyelocytic leukemia (APL) is a blood system disease caused by the accumulation of a large number of immature blood cells in bone marrow. Although the introduction of all-trans retinoic acid (ATRA) and arsenic has reached a high level of complete remission rate and 5-year disease-free survival rate, the occurrence of various adverse reactions still severely affects the quality of life of patients. As a natural product, honokiol (HNK) has the advantages of low toxicity and high efficiency, and it is a potential drug for the treatment of cancer. Since cancer cells can escape apoptotic cell death through multiple adaptive mechanisms, HNK, a drug that induces cancer cell death in a nonapoptotic way, has attracted much interest. We found that HNK reduced the viability of human APL cell line (NB4 cells) by inducing paraptosis-like cell death. The process was accompanied by excessive reactive oxygen species (ROS), mitochondrial damage, endoplasmic reticulum stress, and increased microtubule-associated protein 1 light chain 3 (LC3) processing. The inactivation of proteasome activity was the main cause of misfolded and unfolded protein accumulation in endoplasmic reticulum, such as LC3II/I and p62. This phenomenon could be alleviated by adding cycloheximide (CHX), a protein synthesis inhibitor. We found that mTOR signaling pathway participated in paraptosis-like cell death induced by HNK in an autophagy-independent process. Moreover, the mitogen-activated protein kinase (MAPK) signaling pathway induced paraptosis of NB4 cells by promoting endoplasmic reticulum stress. In summary, these findings indicate that paraptosis may be a new way to treat APL, and provide novel insights into the potential mechanism of paraptosis-like cell death.
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Lee, Hong-Jae, Dong-Min Lee, Min-Ji Seo, Ho-Chul Kang, Seok-Kyu Kwon, and Kyeong-Sook Choi. "PSMD14 Targeting Triggers Paraptosis in Breast Cancer Cells by Inducing Proteasome Inhibition and Ca2+ Imbalance." International Journal of Molecular Sciences 23, no. 5 (February 28, 2022): 2648. http://dx.doi.org/10.3390/ijms23052648.

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PSMD14, a subunit of the 19S regulatory particles of the 26S proteasome, was recently identified as a potential prognostic marker and therapeutic target in diverse human cancers. Here, we show that the silencing and pharmacological blockade of PSMD14 in MDA-MB 435S breast cancer cells induce paraptosis, a non-apoptotic cell death mode characterized by extensive vacuolation derived from the endoplasmic reticulum (ER) and mitochondria. The PSMD14 inhibitor, capzimin (CZM), inhibits proteasome activity but differs from the 20S proteasome subunit-inhibiting bortezomib (Bz) in that it does not induce aggresome formation or Nrf1 upregulation, which underlie Bz resistance in cancer cells. In addition to proteasome inhibition, the release of Ca2+ from the ER into the cytosol critically contributes to CZM-induced paraptosis. Induction of paraptosis by targeting PSMD14 may provide an attractive therapeutic strategy against cancer cells resistant to proteasome inhibitors or pro-apoptotic drugs.
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Wepsic, H. Terry, and Neil Hoa. "Paraptosis and tumor immunity." International Immunopharmacology 114 (January 2023): 109491. http://dx.doi.org/10.1016/j.intimp.2022.109491.

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Yang, Min Hee, In Jin Ha, Seok-Geun Lee, Junhee Lee, Jae-Young Um, Gautam Sethi, and Kwang Seok Ahn. "Brassinin Induces Apoptosis, Autophagy, and Paraptosis via MAPK Signaling Pathway Activation in Chronic Myelogenous Leukemia Cells." Biology 12, no. 2 (February 14, 2023): 307. http://dx.doi.org/10.3390/biology12020307.

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Brassinin (BSN), a potent phytoalexin found in cruciferous vegetables, has been found to exhibit diverse anti-neoplastic effects on different cancers. However, the impact of BSN on chronic myelogenous leukemia (CML) cells and the possible mode of its actions have not been described earlier. We investigated the anti-cytotoxic effects of BSN on the KBM5, KCL22, K562, and LAMA84 CML cells and its underlying mechanisms of action in inducing programmed cell death. We noted that BSN could induce apoptosis, autophagy, and paraptosis in CML cells. BSN induced PARP cleavage, subG1 peak increase, and early apoptosis. The potential action of BSN on autophagy activation was confirmed by an LC3 expression and acridine orange assay. In addition, BSN induced paraptosis through increasing the reactive oxygen species (ROS) production, mitochondria damage, and endoplasmic reticulum (ER) stress. Moreover, BSN promoted the activation of the MAPK signaling pathway, and pharmacological inhibitors of this signaling pathway could alleviate all three forms of cell death induced by BSN. Our data indicated that BSN could initiate the activation of apoptosis, autophagy, and paraptosis through modulating the MAPK signaling pathway.
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Tripathy, Suman Kumar, Umasankar De, Niranjan Dehury, Paltan Laha, Manas Kumar Panda, Hyung Sik Kim, and Srikanta Patra. "Cyclometallated iridium complexes inducing paraptotic cell death like natural products: synthesis, structure and mechanistic aspects." Dalton Transactions 45, no. 38 (2016): 15122–36. http://dx.doi.org/10.1039/c6dt00929h.

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Dissertations / Theses on the topic "Paraptosi"

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RAIMONDI, MICHELA. "THE KEY ROLE OF MITOCHONDRIA IN HUMAN MELANOMA CELLS: A TARGET OF DELTA-TOCOTRIENOL ANTI-CANCER ACTIVITY AND A STEMNESS MARKER." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/816647.

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Malignant melanoma is one of the most aggressive and treatment resistant cancers. Treatment options include surgery, chemotherapy, immunotherapy and targeted therapies. Unfortunately, the large heterogeneity of melanomas and the presence of stem cells within the tumor mass are the main causes of treatment resistance. Natural compounds have attracted great interest in cancer research for their capability to induce paraptosis, a non-canonical cell death characterized by endoplasmic reticulum (ER) dilatation, mitochondrial swelling, reactive oxygen species (ROS) production and Ca++ overload. Accumulating evidence supported the anticancer effect of tocotrienols (TTs); aim of this study was to investigate whether δ-TT might induce paraptosis in A375 and BLM human melanoma cells. We demonstrated that δ-TT induces paraptosis in melanoma cells, causing ER dilatation, mitochondria swelling and the activation of MAPKs. This effect was accompanied by an impairment of mitochondrial function, resulting in a reduction in OXPHOS levels, oxygen consumption, mitochondrial activity and energy depletion. This dysfunction leads to mitochondrial ROS production and increase in Ca++ levels. We then focused our attention on A375 stem cells. Cancer stem cells (CSCs) are a small tumor subpopulation responsible for chemotherapy resistance and they have been reported to be coupled with metabolic alterations. Melanoma SCs deriving from the A375 cell line are characterized by the expression of the ABCG2 transporter and δ-TT treatment counteracts A375 SCs growth. In this work we observed that melanoma SCs are characterized by higher mitochondrial mass, increased OXPHOS, increased PGC1α expression levels and increased mitochondrial fusion markers. We then analyzed whether δ-TT might affect stem cell mitochondria and we observed that δ-TT significantly impairs mitochondrial protein levels. Finally, preliminary data demonstrate that δ-TT affects mitochondria also in vemurafenib-resistant A375 cells. Taken together, all these data demonstrate that 1) δ-TT induces paraptotic cell death in melanoma cells, involving mitochondrial dysfunction, ROS production and Ca++ overload; 2) mitochondrial mass could be considered a novel marker to identify melanoma SCs; 3) δ-TT targets melanoma SCs affecting mitochondrial functions 4) δ-TT impairs mitochondria in vemurafenib-resistant A375 cells.
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Nicolier, Magali. "Induction de l'apoptose de cellules tumorales par la staurosporine : la mitochondrie au carrefour de la mort." Besançon, 2009. http://www.theses.fr/2009BESA0004.

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La mort cellulaire programmée est un processus physiologique basique regroupant de nombreux types de mort dont le principal est l'apoptose. Un défaut de mort cellulaire est fréquemment impliqué dans les développements précoces de cancer et la résistance tumorale aux chimio- et radio-thérapies. Une approche thérapeutique efficace consiste donc à restaurer ces voies de mort court-circuitées dans les cellules tumorales. Dans ce contexte, les protéines kinases sont des cibles prometteuses pour le développement de nouvelles drogues chimiothérapeutiques. Parmi elles, les protéines kinases C (PKC) sont impliquées dans de nombreuses voies de signalisation contrôlant la prolifération cellulaire, la différenciation mais aussi l'apoptose. La staurosporine (STS), un puissant inhibiteur de protéines kinases, dispose non seulement d'une forte activité anti-proliférative, mais est aussi capable d'activer l'apoptose de nombreuses lignées cellulaires tumorales. Des travaux précédents au laboratoire ont montré que la STS induit l'apoptose de lignées dérivées de cancer du col de l'utérus (p53wt HPV+ vs p53 mt HPV-), apoptose impliquant la voie intrinsèque ou mitochondriale. Nous avons montré que la protéine p53 joue un rôle primordial dans cette apoptose et ce, grâce à son activité transcriptionnelle ainsi que son activité mitochondriale indépendante de la transcription. Par ailleurs, nous avons montré que les acteurs impliqués en aval de la voie mitochondriale entraînent la mort des cellules via des voies distinctes, à savoir le cytochrome c et la caspase, et, l'AIF et la voie indépendante des caspases médiée par PARP-1. Ces deux voies ne sont pas activées au même moment selon le statut de p53 (sauvage vs mutée). Les résultats présentés dans ce travail démontrent que la STS ou un de ses dérivés, notamment UCN-01, pourraient être utilisés, seuls ou en combinaison avec d'autres molécules, afin de proposer de nouvelles stratégies anti-cancéreuses visant à éliminer les tumeurs du col de l'utérus via l'activation de la voie apoptotique mitochondriale
Programmed cell death is a group of basic physiological process, the principal one been apoptosis. A fault in this pathway is frequently complicated in both the development of tumors and their resistance to radio- and chemotherapy. However one effective therapeutic approach consists of restoring this pathway in tumors. With this context, protein tumors offer a processing target for drug development. In particular protein kinases C (PKC) are involved in several signaling pathways controlling proliferation differentiation and apoptosis. Staurosporine (STS) is a powerful inhibitor of proteins tumors capable of arresting proliferation and inducing apoptosis in numerous tumoral cell lines. Previous work in our laboratory has shown that STS induces apoptosis in cervical cancer lines (p53wt HPV+ vs p53mt HPV-) by the intrinsic apoptotic pathway. We have demonstrated that p53 plays a pivotal role in apoptose and its transcriptional activity is independent on its mitochondrial effect. In addition, we showed that cell death caused by mitochondrial effects can be achieved by molecules involved in two distinct pathways, the cytochrome c and the caspase cascade, and, AIF and a pathway independent of caspases mediated by PARP-1. The two routes are not activated at the same time according to the status of p53 (wild type vs mutant). The results presented here indicate that STS and more notably ist derivative UCN-01 may be used in future alone or in combination with other molecules to open new fields from the therapeutic intervention of cervical cancers by activating the mitochondrial apoptotic pathway
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FONTANA, FABRIZIO. "APOPTOSIS AND PARAPTOSIS, INVOLVING ENDOPLASMIC RETICULUM STRESS, AUTOPHAGY AND MITOCHONDRIAL DYSFUNCTION, ARE INDUCED BY DELTA-TOCOTRIENOL IN PROSTATE CANCER CELLS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/699447.

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Castration resistant prostate cancer (CRPC) is the most aggressive form of prostate cancer with still limited therapeutic outcomes due to the development of resistance to standard treatments. Unraveling the molecular mechanisms at the basis of the pro-death activity of novel anticancer compounds is necessary to increase the treatment strategies for this pathology. Here, we demonstrated that δ-tocotrienol (δ-TT, a vitamin E derivative) can induce apoptosis in human CRPC cell lines (PC3 and DU145) through modulation of the endoplasmic reticulum (ER) stress-autophagy axis. In these cells, δ-TT also triggers paraptosis, a non-canonical cell death mechanism characterized by cytoplasmic vacuolation resulting from mitochondrial/ER swelling and requiring protein synthesis. Mechanistically, we observed that δ-TT downregulates OXPHOS protein levels and inhibits mitochondrial respiration in PC3 and DU145 cells, leading to reduced oxygen consumption, ATP depletion and AMPK activation. Moreover, δ-TT treatment resulted in Ca2+ homeostasis alteration and ROS production, followed not only by apoptosis/paraptosis but also by mitochondrial fission and mitophagy. Taken together, these data demonstrate that in CRPC δ-TT can trigger both apoptosis and paraptosis, involving ER stress and autophagy. In addition, they suggest that δ-TT specifically alters mitochondrial morphology and function, inducing Ca2+ overload- and oxidative stress-mediated cell death.
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Chose, Olivier. "Développement de nouveaux modèles in vivo pour l'étude de deux processus majeurs de la tumorigenèse : La métastase et l'apoptose." Compiègne, 2003. http://www.theses.fr/2003COMP1462.

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La tumorigenèse est un processus composé de multiples étapes reflétant diverses altérations du génome susceptibles de perturber les voies de prolifération, de différenciation et de mort cellulaire. D'un point de vue clinique, l'émergence des métastases constitue l'étape critique de ce processus. Notre objectif a donc été de tenter de caractériser les cellules tumorales à un stade "pré-métastatique", afin d'identifier de nouveaux marqueurs utilisables en diagnostic précoce ou pour la thérapie. Nous avons étudié le processus métastatique par l'intermédiaire d'un modèle in ovo (membrane chorioallantoi͏̈de d'œuf embryonné de poule), lequel nous a permis de caractériser l'efficacité d'intravasation de diverses lignées cellulaires (myélomes et hybridomes de souris syngéniques). Nous avons pu montrer que ces lignées présentent des capacités métastatiques différentes. L'étude a été complétée par des méthodologies in vitro. Une analyse comparative de l'expression de 1176 gènes associés au cancer nous a conduit par ailleurs à mettre en évidence plusieurs voies cellulaires dont la dérégulation pourraient être associée à un phénotype métastatique précoce. Chez les métazoaires, la machinerie apoptotique s'oppose in vivo aux dérives prolifératives liées à l'émergence des métastases. La mitochondrie est fortement impliquée dans ce processus. La caractérisation des mécanismes de mort cellulaire programmée (MCP), est donc un élément clé dans la stratégie anti-cancéreuse. Afin de tenter d'ouvrir de nouvelles voies d'approches dans ce domaine, les phénomènes de MCP ont été étudiés chez certains organismes dépourvus de mitochondries. Nous avons ainsi pu mettre en évidence chez T. Vaginalis ou G. Intestinalis, une forme de MCP distincte de la nécrose, similaire mais non identique à celles décrites pour les organismes pourvus de mitochondries. Cette découverte ouvre d'intéressantes perspectives tant au niveau moléculaire qu'au niveau évolutif.
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Farinas, Benoît. "L'algue Ostreococcus tauri, modèle émergent pour la caractérisation des principaux acteurs du cycle de division et de la mort cellulaire programmée dans la lignée verte." Perpignan, 2006. http://www.theses.fr/2006PERP0699.

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L'algue marine unicellulaire Ostreococcus tauri (Prasinophycée) a émergé très tôt dans l'évolution de la lignée verte. Elle possède une organisation cellulaire simple, un mode de division par fission binaire et un ensemble minimal de gènes pour la régulation du cycle cellulaire. Une recherche d'hétérotrophie a été menée pour s'affranchir de l'éclairement mais aucun composé carboné testé n'a permis d'observer une prolifération de l'algue. Seul le glycérol a montré une survie prolongée des cultures mises au noir, toutefois sans division des cellules. Dans tous les cas, une mort cellulaire est observée et l'étude de cette mortalité pourrait révéler une mort cellulaire programmée. Plusieurs outils ont été développés pour optimiser la culture de l'algue, et pour étudier l'expression de ses gènes. Une culture axénique, dont la synchronisation naturelle de la division cellulaire par des alternance jour/nuit, a constitué une avancée nécessaire à la caractérisation du cycle cellulaire. La division d'O. Tauri s'est révélée comparable à une division typique eucaryote. OtCDKA, au motif PSTAIRE, est présente et a un rôle dans la régulation de la division. Protéines comme ARNm sont présents de façon constitutive mais OtCDKA possède une activité histone H1 kinase à la transition G1/S, voire G2/M. Comme chez les végétaux, une CDK de type B est exprimée et active durant la division d'O. Tauri, avec une activité plus tardive que OtCDKA. L'essentiel de son action se situe à la transition G2/M pour l'entrée en mitose. Alors que des phosphorylations inhibitrices sont observées chez les CDK PSTAIRE animales pour bloquer l'entrée en phase M, OtCDKB et non OtCDKA est phosphorylée sur tyrosine
The unicellular marine alga Ostreococcus tauri (Prasinophyceae) diverged early in evolution of green plants. O. Tauri has a very simple cellular organisation, a simple binary division and a minimal yet complete set of cell cycle control genes. Heterotrophic growth in darkness was investigated but no proliferation of O. Tauri was observed with the carbon sources tested. However, glycerol increased survival in the dark, albeit without cell division. In all conditions, cell death was observed and our results suggest occurrence of programmed cell death. Cell culture techniques were developed to optimise further work, for example for gene expression studies. Axenic cultures, with natural synchronisation by light/dark cycles was necessary for studying cell cycle regulation. O. Tauri division appeared to be fairly typical of eukaryotes. A PSTAIRE-type CDK (CDKA in plants) in the O. Tauri genome was found to be implicated in cell division. The relevant mRNA and proteins were present constitutively but with a peak of histone H1 activity early in cell cycle, suggesting a role in the G1/S transition and perhaps in the G2/M transition. As in other members of the plant kingdom, O. Tauri possesses a B-type CDK, highly regulated throughout the cell cycle, with a kinase activity occurring after OtCDKA activation, suggesting a mitotic role of OtCDKB. Although the PSTAIRE-type CDK is phosphorylated to inhibit the G2/M transition in animals, surprisingly, a tyrosine phosphorylation was detected only on OtCDKB
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Bardin, Thierry. "Études de motifs de signalisation amyloïde des bactéries aux champignons filamenteux." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0274.

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Une grande variété de voies de signalisation impliquées dans les défenses de l’hôte sont basées sur des mécanismes de transduction du signal de type prion et mettent en jeu des complexes oligomériques appelés signalosomes. Certaines voies utilisant la transmission d’un repliement amyloïde à partir d’un récepteur de type Nod-like (NLR) vers un ou plusieurs effecteurs contrôlant des processus de mort cellulaire programmée ont été décrites chez les champignons filamenteux. Chez Podospora anserina, deux voies de ce type basées sur des motifs amyloïdes appelés HRAM étaient déjà connues. Dans ce travail nous avons caractérisé une troisième voie de signalisation amyloïde induisant la mort impliquant un NLR, PNT1, et un effecteur, HELLP, basé sur le motif amyloïde PP précédemment identifié chez Chaetomium globosum. Nous avons montré que le motif PP forme un prion nommé [pi] capable de déclencher l’activité toxique de la protéine HELLP. Il n’y a aucune interaction croisée avec les deux autres voies de transduction du signal amyloïde de P. anserina, toutes sont indépendantes.Il avait été suggéré sur la base d’homologie de séquences que les motifs PP seraient apparentés aux motifs RHIM trouvés dans les kinases RIPK1 et RIPK3 contrôlant la nécroptose chez les mammifères. Nous avons montré ici que les motifs RHIM humains se propagent sous forme de prions, appelés [Rhim], in vivo chez P. anserina et sont capables d’interagir partiellement avec les prions [pi] démontrant ainsi une homologie fonctionnelle et probablement structurale au moins partielle entre ces motifs. Enfin, une recherche bioinformatique de motifs amyloïdes RHIM-like dans le règne du vivant a révélé la présence de tels motifs uniquement dans des bactéries filamenteuses dans des configurations géniques similaires à celles des systèmes de signalisation amyloïde fongiques (gènes adjacents NLR putative/effecteur). Ces motifs ont été regroupés en dix familles. Tous les motifs testés ont formé des prions in vivo chez P. anserina, certains interagissent partiellement avec les prions [pi] et [Rhim], et les motifs des tandems NLR/effecteur cross-seed renforçant l’hypothèse de l’existence d’une signalisation amyloïde chez les procaryotes multicellulaires.Tous ces résultats suggèrent une conservation évolutive de mécanismes de transduction du signal basé sur une transmission amyloïde associés à des processus de mort cellulaire programmée sur de très longues périodes allant des bactéries, aux champignons et jusqu’aux animaux
A large variety of signaling pathways with roles in host defense are based on prion-like signal transduction mechanisms involving oligomeric complexes termed signalosomes. Some of them using amyloid fold transmission from a Nod-like receptor (NLR) to one or several effectors controlling programmed cell death have been described in filamentous fungi. In Podospora anserina, two such pathways based on motifs termed HRAM were already known. In the present work, we characterized a third death inducing amyloid signaling pathway involving a NLR, PNT1, and an effector, HELLP, based on the PP amyloid motif previously identified in Chaetomium globosum. We showed that the PP motif forms a prion termed [pi], which can trigger HELLP toxic activity. There is no cross-interaction with the two other P. anserina amyloid signaling pathways, they are all independent.Based on sequence homologies, it was formerly outlined that PP-motif could be related to RHIM motifs found in RIPK1 and RIPK3 kinases controlling necroptosis in mammals. In this work, we showed that human RHIM motifs propagate as prions, termed [Rhim], in vivo in P. anserina and can partially cross-interact with [pi] prions therefore demonstrating at least a partial functional and probably structural homology between these motifs. Finally, bioinformatic studies aiming to find RHIM-like amyloid motifs in living organisms revealed the presence of such motifs uniquely in filamentous bacteria in genes layout similar to fungal amyloid signaling systems (adjacent genes encoding putative NLR/effector). These motifs were grouped in ten families. All the tested motifs formed prions in vivo in P. anserina, some of them partially interact with [pi] and [Rhim] prions, and the motifs of NLR/effector tandems cross seed reinforcing the hypothesis of amyloid signaling in Prokaryotes.Altogether, these results suggest conservative evolution of amyloid based signal transduction associated to programmed cell death over very long period from bacteria to fungi and to mammals
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Bury, Marina. "Caractérisation des propriétés anticancéreuses de la fusicoccine A et de l'ophioboline A au sein de modèles expérimentaux de glioblastomes humains." Doctoral thesis, Universite Libre de Bruxelles, 2013. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209483.

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Le glioblastome est la plus fréquente et la plus agressive des tumeurs cérébrales primaires.

Malgré un traitement standard pluridisciplinaire (chirurgie, radiothérapie et chimiothérapie),

la médiane de survie des patients atteints de ce type de tumeur est de 15 mois et aucun patient

n’a pu être guéri à ce jour. Ce pronostic très sombre est directement lié à la capacité

d’invasion diffuse du parenchyme cérébral par les cellules gliales tumorales, ce qui rend

impossible une résection chirurgicale totale. De plus, ces cellules sont particulièrement

résistantes aux traitements chimiothérapeutiques de type pro-apoptotique, entrainant une

récidive quasi inévitable de la tumeur. De nombreuses stratégies thérapeutiques telles que

l’immunothérapie ou les thérapies ciblées sont actuellement explorées pour tenter de

combattre ces tumeurs. Cependant, leur efficacité au niveau clinique s’est avérée décevante. Il

devient donc indispensable d’identifier de nouveaux agents thérapeutiques afin d’améliorer la

survie des patients atteints de glioblastome.

Dans ce travail, nous avons caractérisé les propriétés anticancéreuses in vitro et in vivo de

deux terpénoïdes extraits de champignons, la fusicoccine A et l’ophioboline A, puis nous

avons caractérisé en partie leur mécanisme d’action anti-tumoral dans des cellules de

glioblastome.

Tout d’abord, nous avons montré que l’activité inhibitrice de croissance in vitro de la

fusicoccine A et de l’ophioboline A n’était pas dépendante du degré de sensibilité ou de

résistance à l’apoptose des cellules gliales tumorales. Nous avons ensuite mis en évidence que

la fusicoccine A était capable de diminuer l’invasion des cellules de glioblastome in vitro en

ciblant la kinase focale d’adhérence (FAK). Dans le même temps, nous avons démontré que

l’ophioboline A était capable d’induire la mort de ces cellules par paraptose en inhibant

l’activité du canal ionique BKCa. Ces deux cibles sont intéressantes car en plus d’être

surexprimées dans les glioblastomes, elles interviennent dans de nombreux processus

cellulaires tels que la prolifération, la migration et la survie cellulaire.

Pour finir, nous avons analysé le pouvoir anti-tumoral in vivo de ces deux terpénoïdes en

utilisant un modèle murin de mélanome métastatique, couramment utilisé dans notre

laboratoire. Seule l’ophioboline A, injectée en intrapéritonéal à 10 mg/kg, augmentait de

manière significative la survie des souris traitées avec cette molécule par rapport aux souris

contrôles. Dans ce premier modèle, nous n’avions pas déterminé les conditions optimales

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pour l’évaluation in vivo de la fusicoccine A et de l’ophioboline A. Lorsque celles-ci seront

définies, des modèles de xénogreffes orthotopiques de glioblastomes humains implantées dans

le cerveau de souris immunodéficientes seront utilisés.

En conclusion, l’ophioboline A, pouvant être produite en quantités industrielles par culture

du champignon qui la synthétise, possédant un mécanisme d’action original et montrant déjà

un début d’activité in vivo, pourrait représenter une molécule méritant des études plus

approfondies en termes d’agent thérapeutique susceptible de combattre les glioblastomes.
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Beaugelin, Ines. "Caractérisation de médiateurs de la signalisation de l'oxygène singulet chez les plantes conduisant à la mort cellulaire ou à la tolérance à la forte lumière." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0609.

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L’oxygène singulet ($^1O_2$) est la principale espèce réactive de l’oxygène produite dans le chloroplaste lors d'un stress photo-oxydant. L’$^1O_2$ est hautement cytotoxique s'attaquant aux protéines et lipides membranaires. L’$^1O_2$ est une molécule signal impliquée dans une signalisation rétrograde entre les chloroplastes et le noyau via des médiateurs, menant à la mort cellulaire programmée (MCP), ou à l’acclimatation. Nous avons caractérisé l’implication de la phytohormone salicylate, agissant en aval de la signalisation de la MCP dépendante d’OXI1 (OXIDATIVE SIGNAL INDUCIBLE 1) et du jasmonate. Nous avons mis en évidence une voie de régulation négative faisant intervenir des protéines inhibitrices de la MCP : DAD1 et DAD2. La sur-expression de ces protéines permet à la plante d’éviter de la MCP en inhibant la signalisation contrôlée par OXI1. Dans le Réticulum Endoplasmique (RE) a lieu la conformation d’une grande partie des protéines. Une perturbation dans ce compartiment induit l’activation d’une réponse adaptative appelée l’UPR (Unfolded Protein Response). Nous avons monté que la production d’$^1O_2$ active l’UPR. L’acclimatation à la forte lumière (FL) fait intervenir la branche bZIP28/BiP3 de l’UPR. Un pré-traitement modéré d’un inducteur de stress RE (tunicamycine), induisant l'UPR, déclenche une réponse d’acclimatation à l’$^1O_2$ permettant l’évitement de la MCP lors de l’exposition à la FL. Nous avons réalisé un crible génétique pour rechercher des révertants du mutant \textit{ch1} (un surproducteur d’1$^1O_2$) où l’inhibition de la croissance par l’$^1O_2$ est partiellement levée. Les gènes candidats identifiés feront l’objet d’études complémentaires
Singlet oxygen ($^1O_2$) is a major reactive oxygen species produced within the chloroplasts during high light (HL) stress. $^1O_2$ has a cytotoxic effect due to its high reactivity towards macromolecules including proteins and membrane lipids. $^1O_2$ also acts as a signal molecule that plays a role in chloroplast-to-nucleus retrograde signaling involving mediators and leading either to programmed cell death (PCD) or to stress acclimation.We have shown the involvement of the phytohormone salicylic acid in HL-induced cell death, acting downstream of the OXI1 kinase and jasmonate. We have also shown a negative regulation of this signaling pathway by PCD inhibitory proteins: DAD1 and DAD2 (DEFENDER AGAINST CELL DEATH 1 and 2). Overexpressing those proteins inhibits OXI1-mediated PCD. Protein folding of most secreted proteins takes place in the Endoplasmic Reticulum (ER). Perturbations in this compartment lead to the activation of an adaptive response called UPR (Unfolded Protein Response). When ER stress is too intense, NRPs-mediated ER stress-induced cell death is activated. We have shown that 1O2 production activates UPR. In particular, the bZIP28/BiP3 UPR branch is activated during acclimation to HL. The induction of UPR by a chemical inducer of ER stress (Tunicamycin) can induce acclimation to $^1O_2$ production and can avoid HL-induced PCD.We performed a genetic screen to search for revertants of the $^1O_2$ overproducing \textit{ch1} mutants in which growth inhibition by$^1O_2$2 is partially released. The candidate genes will have to be confirmed by further phenotypic studies
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Kremer, Natacha. "Évolution de la dépendance dans les symbioses à Wolbachia : étude du genre Asobara (Hymenoptera : braconidae)." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10141.

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Les associations entre organismes eucaryotes et micro-organismes sont fréquemment observées dans la nature et s’étendent le long du continuum parasitisme-mutualisme. Si de nombreuses associations symbiotiques ont été bien caractérisées, leur mise en place et leur évolution ont été rarement étudiées. Les bactéries intracellulaires Wolbachia induisent des effets très différents, variant du parasitisme de la reproduction chez les Arthropodes au mutualisme chez les Nématodes. Nous nous sommes ici intéressés à l’hyménoptère Asobara tabida, rare espèce où Wolbachia est obligatoire pour l’ovogenèse de son hôte Arthropode, de façon à étudier les mécanismes à l’origine d’une transition évolutivement récente. Nous avons tout d’abord étudié la variabilité de la dépendance vis-à-vis de Wolbachia au sein du genre Asobara. Par diverses approches de transcriptomique, nous avons ensuite caractérisé les mécanismes moléculaires impliqués dans la dépendance chez A. tabida, et mis en évidence des processus impliqués dans la mort cellulaire programmée, l’immunité (sens large) et le développement. Enfin, nous avons étudié l’impact de Wolbachia sur la physiologie de son hôte, en étudiant le métabolisme du fer et plus généralement l’immunité dans diverses associations symbiotiques. Ces études montrent que la dépendance n’est pas forcément associée à l’apport de nouvelles fonctions et pourrait au contraire être le reflet de processus compensatoires mis en place par l’hôte, en réponse aux perturbations physiologiques induites par le symbiote. Ces résultats appellent à considérer les effets et les conséquences de ces symbiotes au delà des mécanismes qui permettent leur maintien dans les populations
Associations between eukaryotes and micro-organisms are frequently observed in nature and range along the continuum between parasitism and mutualism. Numerous associations have already been well described; however the origin and the evolution of these associations are rarely studied. We focused on the intracellular bacterium Wolbachia, which induces very different phenotypic effects, ranging from facultative reproductive parasitism in Arthropods to obligatory mutualism in Nematodes. Here we studied the hymenopteran Asobara tabida, a rare species in which Wolbachia is necessary for oogenesis completion of its Arthropod host, in order to investigate the mechanisms underlying an evolutionarily recent transition. We first studied the variability of dependence to Wolbachia within the Asobara genus. Using various transcriptomic approaches, we next characterized molecular echanisms involved in dependence between A. tabida and Wolbachia, and highlighted processes implicated in programmed cell death, immunity (broad sense) and development. Finally, we examined to what extent Wolbachia impacts host physiology, by studying iron metabolism and global immunity in various symbiotic associations. These studies highlight that dependence is not always linked with the provision of a new function. It could rather reflect host compensatory mechanisms in response to physiological perturbations induced by the presence of symbiont. More generally, these results invite to consider the effects and the consequences of symbionts over the mechanisms allowing their persistence within populations
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TSAI, CHONG-BIN, and 蔡忠斌. "Fenofibrate Induces Lipogenesis and Paraptosis of MCF-7 Breast Cancer Cells." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/gm6a2p.

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博士
國立中正大學
生命科學系分子生物研究所
105
Breast cancer is the most common invasive cancer in women worldwide. Conventional breast cancer therapies include surgical resection, radiotherapy, and chemotherapy. Despite the recent development of adjuvant therapies targeting estrogen and growth factor pathways, the incidence of breast cancer has not declined. Therefore, the search for new therapeutic targets and treatment modalities are necessary. One of the strategies of effective cancer therapy is induction of cell death of cancer cells using various cytotoxic agents. Apoptosis is the most well-known modality of cell death. In 2000, Sperandio et al. described a form of programmed cell death called paraptosis, which is morphologically and biochemically distinct from apoptosis. Paraptosis was associated with extensive cytoplasmic vacuolization and mitochondrial swelling, but without any other morphological hallmark of apoptosis. The other important strategy of cancer therapy, Pierce introduced the concept of differentiation therapy that malignant cells can differentiate into non-malignant cells in 1971. The development of differentiation therapy required the identification of targetable pathways to re-activate blocked terminal differentiation programs in cancer cell. Recent studies showed that enhanced expression of PPARs in malignant tissue implicates the possible involvement of PPARs signal pathway in tumorigenesis. It also has been shown that PPARs are involved in cell differentiation programs during development. However, published evidences were mainly on the work of PPARγ. In this research, we focused the fate of MCF7 breast cancer cell after treating with PPARα agonist fenofibrate. The potential anti-proliferative actions of fenofibrate on MCF7 cells were studied through the analyses of inhibition of cell viability, cell cycle analysis, cloning-forming capacity and appearance of cell paraptosis. The differentiation-inducing abilities of fenofibrate were studied through induction of mammary glandular characteristics, including lipid accumulation and casein expression. DNA Microarray analysis was also applied to elucidate the up- and down-regulatory genes affect by fenofibrate treatment. Analyses of differential expressed genes by Ingenuity Pathway Analysis and STRING Database implied the potential ability of fenofibrate to alter cell fate of breast cancer cell was via inhibition of cell cycle and activation of ER stress pathway, esp. PERK pathway. This study outlined the signaling pathway of fenofibrate-induced differentiation and paraptosis of MCF-7 cells. Fenofibrate activated PERK of ER stress, and increased the expression levels of downstream cascade genes, ATF4, ATF3, CHOP and TRB3. TRB3 could inhibit PI3K/Akt cell survival signal to decrease cell viability. In addition, ATF3 associated with p53 to stabilize it, stabilized p53 stimulated p21 expression. Increased p53 and p21 suppressed expression of cyclin D1, CDK4 and CDK6 and ATF3 could also inhibit expression of cyclin D1. Eventually entry of cells into cell cycle S phase was prevented and arrested cells in cell cycle G1/Go phase. The cell cycle arrest might initiate the process of mammary glandular differentiation of MCF-7 cells. On the other hand, TRB3 could also activate MAPK pathway which has been shown to mediate paraptosis.
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Book chapters on the topic "Paraptosi"

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Khalili, Maryam, and James A. Radosevich. "Paraptosis." In Apoptosis and Beyond, 343–66. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119432463.ch16.

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Kessel, David. "Detection of Paraptosis After Photodynamic Therapy." In Methods in Molecular Biology, 711–20. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2099-1_38.

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Tardito, Saverio, Claudio Isella, Enzo Medico, Luciano Marchiò, Maurizio Lanfranchi, Ovidio Bussolati, and Renata Franchi-Gazzola. "Paraptotic Cell Death Induced by the Thioxotriazole Copper Complex A0: A New Tool to Kill Apoptosis-Resistant Cancer Cells." In Platinum and Other Heavy Metal Compounds in Cancer Chemotherapy, 201–7. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-459-3_25.

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"Paraptosis." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1442. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_12304.

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Sperandio, Sabina, and Ian de Belle. "Paraptosis." In Beyond Apoptosis, 157–74. CRC Press, 2008. http://dx.doi.org/10.3109/9781420020502-11.

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Conference papers on the topic "Paraptosi"

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Kessel, David H. "Photodynamic therapy and paraptosis: an update." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXVIII, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2506325.

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Kessel, David H., Won-Jin Cho, and Hyeong-Reh Kim. "Photodynamic therapy: apoptosis, paraptosis, and autophagy." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXIX, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2020. http://dx.doi.org/10.1117/12.2543895.

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Cho, Won-Jin, David H. Kessel, and Hyeong-Rey Kim. "Photodynamic therapy: the role of paraptosis." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXVII, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2018. http://dx.doi.org/10.1117/12.2291997.

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Wang, Chao-yang, and Tong-Sheng Chen. "Taxol-induced paraptosis-like A549 cell death is not senescence." In SPIE BiOS, edited by Wei R. Chen. SPIE, 2011. http://dx.doi.org/10.1117/12.877056.

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Hager, Sonja, Veronika F. Pape, Vivien Pósa, Bianca Montsch, Lukas Uhlik, Gergely Szakàcs, Szilárd Tóth, et al. "Abstract 1939: Improved activity and paraptosis-induction of anticancer thiosemicarbazones requires high copper(II) complex stability and slow reduction kinetics." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1939.

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Wang, Lin, Justin Gundelach, and Richard Bram. "Abstract 4313: Protein synthesis modulates paraptotic death induced by inhibition of cyclophilins in glioblastoma (GBM) cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4313.

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Reisenauer, K., Y. Tao, A. Ingros, T. Philip, A. Evidente, A. Kornienko, D. Romo, and J. Taube. "Abstract P4-07-10: Epithelial-mesenchymal transition sensitizes breast cancer cells to paraptosis-mediated cell death via the fungus-derived sesterpenoid, Ophiobolin A." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-p4-07-10.

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Mandula, Jessica, Shiun Chang, Eslam Mohamed, Rachel Jiminez, Rosa Sierra-Mondragon, Darwin Chang, Alyssa Obermayer, et al. "1420 Targeting endoplasmic reticulum stress-responsive PERK in melanoma elicits paraptosis-mediated immunogenic cell death and induction of type I interferon-dependent adaptive antitumor immunity." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1420.

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