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Accumulation of P53 and Reductions in XIAP Abundance Promote the Apoptosis of Prostate Cancer Cells
Research Article Accumulation of p53 and Reductions in XIAP Abundance Promote the Apoptosis of Prostate Cancer Cells Subhra Mohapatra, Baoky Chu, Xiuhua Zhao, and W.J. Pledger Department of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center and Research Institute and the University of South Florida Medical Center, Tampa, Florida Abstract activates caspase-9. Most drugs signal apoptosis through the Toward the goal of developing effective treatments for mitochondrial pathway. prostate cancers, we examined the effects of cyclin-dependent Proteins that modulate caspase activity and thus determine kinase inhibitors on the survival of prostate cancer cells. We whether cells live or die include the inhibitor of apoptosis proteins show that roscovitine, R-roscovitine, and CGP74514A (collec- (IAPs) and the Bcl-2 proteins. The IAP family includes cIAP-1, cIAP- tively referred to as CKIs) induce the apoptosis of LNCaP and 2, XIAP, and survivin (11). Of these proteins, XIAP is the most potent. LNCaP-Rf cells, both of which express wild-type p53. Apoptosis IAPs interact with and inhibit the activity of processed caspases; required caspase-9 and caspase-3 activity, and cytochrome c thus, they function as ‘‘brakes’’ that can impede the apoptotic accumulated in the cytosol of CKI-treated cells. Amounts of process once it begins. IAPs inactivate both initiator and effector caspases; caspase-9 and caspase-3 are IAP targets, whereas caspase- p53 increased substantially in CKI-treated cells, whereas amounts of the endogenous caspase inhibitor XIAP decreased. 8 is not (12). CKIs did not appreciably induce the apoptosis of LNCaP cells The Bcl-2 proteins are critical determinants of mitochondria- treated with pifithrin-A, which prevents p53 accumulation, or dependent caspase activation (13). -
The Role of RNA Editing in Cancer Development and Metabolic Disorders
Washington University School of Medicine Digital Commons@Becker Open Access Publications 2018 The oler of RNA editing in cancer development and metabolic disorders Che-Pei Kung Washington University School of Medicine in St. Louis Leonard B. Maggi Jr. Washington University School of Medicine in St. Louis Jason D. Weber Washington University School of Medicine in St. Louis Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Kung, Che-Pei; Maggi, Leonard B. Jr.; and Weber, Jason D., ,"The or le of RNA editing in cancer development and metabolic disorders." Frontiers in endocrinology.9,. 762. (2018). https://digitalcommons.wustl.edu/open_access_pubs/7400 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. REVIEW published: 18 December 2018 doi: 10.3389/fendo.2018.00762 The Role of RNA Editing in Cancer Development and Metabolic Disorders Che-Pei Kung 1,2*, Leonard B. Maggi Jr. 1,2 and Jason D. Weber 1,2,3* 1 ICCE Institute, Washington University School of Medicine, Saint Louis, MO, United States, 2 Division of Molecular Oncology, Department of Medicine, Washington University School of Medicine, Saint Louis, MO, United States, 3 Siteman Cancer Center, Department of Cell Biology and Physiology, Washington University School of Medicine, Saint Louis, MO, United States Numerous human diseases arise from alterations of genetic information, most notably DNA mutations. Thought to be merely the intermediate between DNA and protein, changes in RNA sequence were an afterthought until the discovery of RNA editing 30 years ago. -
Life, Death, and the Pursuit of Apoptosis
Downloaded from genesdev.cshlp.org on October 4, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW Life, death, and the pursuit of apoptosis Eileen White Center for Advanced Biotechnology and Medicine and Department of Biological Sciences and the Cancer Institute of New Jersey, Rutgers University, Piscataway, New Jersey 08854 USA Apoptosis or programmed cell death is a genetically con- (Oltvai et al. 1993). Bcl-2 is expressed widely during em- trolled response for cells to commit suicide. The symp- bryogenesis (LeBrun et al. 1993; Novack and Korsmeyer toms of apoptosis are viability loss accompanied by cy- 1994), and its expression becomes more restricted in toplasmic boiling, chromatin condensation, and DNA adult tissues to those requiring long-term survival (stem fragmentation (Wyllie 1980). Pathologists and develop- cells, postmitotic neurons, and proliferating zones; mental biologists have cataloged the occurrences of ap- Hockenbery et al. 1991). optosis for many years based on these defined morpho- Apoptosis plays a major role in normal development, logical features, but what has propelled apoptosis into and it was expected that gain- or loss-of-function of a the forefront of basic research has been the identification death inhibitor such as Bcl-2 would have a phenotype in of genes that control cell death and the appreciation of transgenic mice. Bcl-2 was expected to regulate apopto- the role of apoptosis in development and disease. Regu- sis in lymphoid cells because of the role of Bcl-2 in hu- lation of cell death is essential for normal development man B cell lymphoma. Targeted Bcl-2 overexpression to and is an important defense against viral infection and the lymphoid system extends normal B cell survival the emergence of cancer. -
Mohammad Karbaschi Thesis
STRUCTURAL, PHYSIOLOGICAL AND MOLECULAR CHARACTERISATION OF THE AUSTRALIAN NATIVE RESURRECTION GRASS TRIPOGON LOLIIFORMIS (F.MUELL.) C.E.HUBB. DURING DEHYDRATION AND REHYDRATION Mohammad Reza Karbaschi Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy Centre for Tropical Crops and Biocommodities Science and Engineering Faculty Queensland University of Technology November 2015 Keywords Arabidopsis thaliana; Agrobacterium-mediated transformation; Anatomy; Anti-apoptotic proteins; BAG4; Escherichia coli; Bulliform cells; C4 photosynthesis; Cell wall folding; Cell membrane integrity; Chaperone-mediated autophagy; Chlorophyll fluorescence; Hsc70/Hsp70; Desiccation tolerance, Dehydration; Drought; Electrolyte leakage; Freehand sectioning; Homoiochlorophyllous; Leaf structure; Leaf folding; Reactive oxygen species (ROS); Resurrection plant; Morphology; Monocotyledon; Nicotiana benthamiana; Photosynthesis; Physiology; Plant tissue; Programed cell death (PCD); Propidium iodide staining; Protein microarray chip; Sclerenchymatous tissue; Stress; Structure; Tripogon loliiformis; Ubiquitin; Vacuole fragmentation; Kranz anatomy; XyMS+; Structural, physiological and molecular characterisation of the Australian native resurrection grass Tripogon loliiformis (F.Muell.) C.E.Hubb. during dehydration and rehydration i Abstract Plants, as sessile organisms must continually adapt to environmental changes. Water deficit is one of the major environmental stresses that affects plants. While most plants can tolerate moderate dehydration -
Expression of the Tumor Necrosis Factor Receptor-Associated Factors
Expression of the Tumor Necrosis Factor Receptor- Associated Factors (TRAFs) 1 and 2 is a Characteristic Feature of Hodgkin and Reed-Sternberg Cells Keith F. Izban, M.D., Melek Ergin, M.D, Robert L. Martinez, B.A., HT(ASCP), Serhan Alkan, M.D. Department of Pathology, Loyola University Medical Center, Maywood, Illinois the HD cell lines. Although KMH2 showed weak Tumor necrosis factor receptor–associated factors expression, the remaining HD cell lines also lacked (TRAFs) are a recently established group of proteins TRAF5 protein. These data demonstrate that consti- involved in the intracellular signal transduction of tutive expression of TRAF1 and TRAF2 is a charac- several members of the tumor necrosis factor recep- teristic feature of HRS cells from both patient and tor (TNFR) superfamily. Recently, specific members cell line specimens. Furthermore, with the excep- of the TRAF family have been implicated in promot- tion of TRAF1 expression, HRS cells from the three ing cell survival as well as activation of the tran- HD cell lines showed similar TRAF protein expres- scription factor NF- B. We investigated the consti- sion patterns. Overall, these findings demonstrate tutive expression of TRAF1 and TRAF2 in Hodgkin the expression of several TRAF proteins in HD. Sig- and Reed–Sternberg (HRS) cells from archived nificantly, the altered regulation of selective TRAF paraffin-embedded tissues obtained from 21 pa- proteins may reflect HRS cell response to stimula- tients diagnosed with classical Hodgkin’s disease tion from the microenvironment and potentially (HD). In a selective portion of cases, examination of contribute both to apoptosis resistance and cell HRS cells for Epstein-Barr virus (EBV)–encoded maintenance of HRS cells. -
ATP-Binding and Hydrolysis in Inflammasome Activation
molecules Review ATP-Binding and Hydrolysis in Inflammasome Activation Christina F. Sandall, Bjoern K. Ziehr and Justin A. MacDonald * Department of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, 3280 Hospital Drive NW, Calgary, AB T2N 4Z6, Canada; [email protected] (C.F.S.); [email protected] (B.K.Z.) * Correspondence: [email protected]; Tel.: +1-403-210-8433 Academic Editor: Massimo Bertinaria Received: 15 September 2020; Accepted: 3 October 2020; Published: 7 October 2020 Abstract: The prototypical model for NOD-like receptor (NLR) inflammasome assembly includes nucleotide-dependent activation of the NLR downstream of pathogen- or danger-associated molecular pattern (PAMP or DAMP) recognition, followed by nucleation of hetero-oligomeric platforms that lie upstream of inflammatory responses associated with innate immunity. As members of the STAND ATPases, the NLRs are generally thought to share a similar model of ATP-dependent activation and effect. However, recent observations have challenged this paradigm to reveal novel and complex biochemical processes to discern NLRs from other STAND proteins. In this review, we highlight past findings that identify the regulatory importance of conserved ATP-binding and hydrolysis motifs within the nucleotide-binding NACHT domain of NLRs and explore recent breakthroughs that generate connections between NLR protein structure and function. Indeed, newly deposited NLR structures for NLRC4 and NLRP3 have provided unique perspectives on the ATP-dependency of inflammasome activation. Novel molecular dynamic simulations of NLRP3 examined the active site of ADP- and ATP-bound models. The findings support distinctions in nucleotide-binding domain topology with occupancy of ATP or ADP that are in turn disseminated on to the global protein structure. -
Beyond Tumor Necrosis Factor Receptor: TRADD Signaling in Toll-Like Receptors
Beyond tumor necrosis factor receptor: TRADD signaling in toll-like receptors Nien-Jung Chen*†‡, Iok In Christine Chio*‡, Wen-Jye Lin*, Gordon Duncan*, Hien Chau*§, David Katz*¶, Huey-Lan Huang*ʈ, Kelly A. Pike*,**, Zhenyue Hao*, Yu-Wen Su*, Kazuo Yamamoto*, Rene´ e F. de Pooter††, Juan Carlos Zu´ n˜ iga-Pflu¨ cker††, Andrew Wakeham*, Wen-Chen Yeh*, and Tak W. Mak*‡‡ *The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network and Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada M5G 2C1; †Institute of Microbiology and Immunology, School of Life Science, National Yang-Ming University, Taipei, Taiwan 112, Republic of China; and ††Department of Immunology, University of Toronto, Sunnybrook and Women’s College Health Sciences Centre, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5 Contributed by Tak W. Mak, July 9, 2008 (sent for review June 24, 2008) Tumor necrosis factor receptor 1-associated death domain protein tory responses in vivo, but also that this molecule is involved in (TRADD) is the core adaptor recruited to TNF receptor 1 (TNFR1) germinal center (GC) formation, T cell costimulation, and TLR upon TNF␣ stimulation. In cells from TRADD-deficient mice, TNF␣- signaling. Our TRADD knockout mice represent a very useful mediated apoptosis and TNF␣-stimulated NF-B, JNK, and ERK tool for extending the ever-increasing list of TRADD functions activation are defective. TRADD is also important for germinal in vitro and in vivo. center formation, DR3-mediated costimulation of T cells, and TNF␣- mediated inflammatory responses in vivo. TRADD deficiency does Results not enhance IFN␥-induced signaling. -
The UVB-Induced Gene Expression Profile of Human Epidermis in Vivo Is Different from That of Cultured Keratinocytes
Oncogene (2006) 25, 2601–2614 & 2006 Nature Publishing Group All rights reserved 0950-9232/06 $30.00 www.nature.com/onc ORIGINAL ARTICLE The UVB-induced gene expression profile of human epidermis in vivo is different from that of cultured keratinocytes CD Enk1, J Jacob-Hirsch2, H Gal3, I Verbovetski4, N Amariglio2, D Mevorach4, A Ingber1, D Givol3, G Rechavi2 and M Hochberg1 1Department of Dermatology, The Hadassah-Hebrew University Medical Center, Jerusalem, Israel; 2Department of Pediatric Hemato-Oncology and Functional Genomics, Safra Children’s Hospital, Sheba Medical Center and Sackler School of Medicine, Tel-Aviv University,Tel Aviv, Israel; 3Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel and 4The Laboratory for Cellular and Molecular Immunology, Department of Medicine, The Hadassah-Hebrew University Medical Center, Jerusalem, Israel In order to obtain a comprehensive picture of the radiation. UVB, with a wavelength range between 290 molecular events regulating cutaneous photodamage of and 320 nm, represents one of the most important intact human epidermis, suction blister roofs obtained environmental hazards affectinghuman skin (Hahn after a single dose of in vivo ultraviolet (UV)B exposure and Weinberg, 2002). To protect itself against the were used for microarray profiling. We found a changed DNA-damaging effects of sunlight, the skin disposes expression of 619 genes. Half of the UVB-regulated genes over highly complicated cellular programs, including had returned to pre-exposure baseline levels at 72 h, cell-cycle arrest, DNA repair and apoptosis (Brash et al., underscoring the transient character of the molecular 1996). Failure in selected elements of these defensive cutaneous UVB response. -
NLR Members in Inflammation-Associated
Cellular & Molecular Immunology (2017) 14, 403–405 & 2017 CSI and USTC All rights reserved 2042-0226/17 $32.00 www.nature.com/cmi RESEARCH HIGHTLIGHT NLR members in inflammation-associated carcinogenesis Ha Zhu1,2 and Xuetao Cao1,2,3 Cellular & Molecular Immunology (2017) 14, 403–405; doi:10.1038/cmi.2017.14; published online 3 April 2017 hronic inflammation is regarded as an impor- nucleotide-binding and oligomerization domain IL-2,8 and NAIP was found to regulate the STAT3 Ctant factor in cancer progression. In addition (NOD)-like receptors (NLRs). TLRs and CLRs are pathway independent of inflammasome formation.9 to the immune surveillance function in the early located in the plasma membranes, whereas RLRs, The AOM/DSS model is the most popular model stage of tumorigenesis, inflammation is also known ALRs and NLRs are intracellular PRRs.3 Unlike used to study the function of NLRs in fl fl as one of the hallmarks of cancer and can supply other families that have been shown to bind their in ammation-associated carcinogenesis. In amma- the tumor microenvironment with bioactive mole- specific cognate ligands, the distinct ligands for somes initiated by NLRs or AIM2 have been widely cules and favor the development of other hallmarks NLRs are still unknown. In fact, mounting evidence reported to participate in the maintenance of 10,11 Nlrp3 Nlrp6 of cancer, such as genetic instability and angiogen- suggests that NLRs function as cytoplasmic sensors intestinal homeostasis. -/-, -/-, Nlrc4 Nlrp1 Nlrx1 Nlrp12 esis. Moreover, inflammation contributes to the and participate in modulating TLR, RLR and CLR -/-, -/-, -/- and -/- mice are 4 more susceptible to AOM/DSS-induced colorectal changing tumor microenvironment by altering signaling pathways. -
Study on Apoptosis in Human Deciduous Tooth Pulp Cells Original
Yuko Okai et al.: Apoptosis in Human Deciduous Tooth Pulp Cells Journal of Hard Tissue Biology 21[4] (2012) p413-420 © 2012 The Hard Tissue Biology Network Association Printed in Japan, All rights reserved. CODEN-JHTBFF, ISSN 1341-7649 Original Study on Apoptosis in Human Deciduous Tooth Pulp Cells Yuko Okai1), Kyoko Harada1), Kiyoshi Ohura2) and Kenji Arita1) 1)Department of Pediatric Dentistry, Osaka Dental University,Osaka, Japan 2)Department of Pharmacology, Osaka Dental University, Osaka, Japan (Accepted for publication, July 5, 2012) Abstract: Dental pulp plays an important role in tooth vitality. The pulp of deciduous tooth thus shows vigorous metabolism and repeated, vigorous cell regeneration and proliferation. Furthermore, natural, programmed cell death (apoptosis) frequently occurs as part of this cell regeneration and proliferation process. Apoptosis is defined as cell death governed by intracellular signals (active death of the cell triggered by changes in physiological or external conditions), and the birth of new cells occurs simultaneously with cell death. Apoptosis thus functions as a driving force for morphological and other changes in organisms, and is essential for phenomena such as ontogenetic processes or aging. However, In order to clarify the mechanism of apoptosis in the deciduous tooth pulp cells, we used SuperArray analysis and immunostaining to examine both deciduous and permanent tooth pulp cells. Of the 84 major genes involved in apoptosis, seven showed greater expression in the deciduous tooth pulp cells than in the permanent tooth pulp cells. Gene expression of TP53BP2, CRADD, BAK1, BIRC3, CASP8, CASP2 and TP73 in the deciduous tooth pulp were 16.1, 9.0, 8.5, 8.1, 5.9, 5.8 and 3.2 times greater than those in the permanent tooth pulp cells, respectively. -
Hsa-Mir-21-5P
Supporting Information An exosomal urinary miRNA signature for early diagnosis of renal fibrosis in Lupus Nephritis 1 2 2 1 1 Cristina Solé , Teresa Moliné , Marta Vidal , Josep Ordi-Ros , Josefina Cortés-Hernández 1Hospital Universitari Vall d’Hebron, Vall d’Hebron Research Institute (VHIR), Lupus Unit, Barcelona, Spain; [email protected] (C.S); [email protected] (J.O-R.); [email protected] (J.C-H.) 2 Hospital Universitari Vall d’Hebron, Department of Renal Pathology, Barcelona, Spain; [email protected] (T.M); [email protected] (M.V). INDEX 1. SI Materials and Methods......................................................................................3 2. SI References…………………………………………………………………………….7 2. SI Figures................................................................................................................8 4. SI Tables................................................................................................................21 2 SI Materials and Methods Patients and samples Patients with biopsy-proven active LN were recruited from the Lupus Unit at Vall d’Hebron Hospital (N=45). All patients fulfilled at least 4 of the American College of rheumatology (ACR) revised classification criteria for SLE [1]. Healthy donors were used as controls (N=20). Urine samples were collected from each patient 1 day before renal biopsy and processed immediately to be stored at -80ºC. Patients with urinary tract infection, diabetes mellitus, pregnancy, malignancy and non-lupus-related renal failure were excluded. In addition, key laboratory measurements were obtained including complement levels (C3 and C4), anti-double-stranded DNA (anti-dsDNA), 24-h proteinuria, blood urea nitrogen (BUN), serum creatinine and the estimated glomerular filtration ratio (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula [2]. SLE disease activity was assessed by the SLE Disease Activity Index 2000 update (SLEDAI-2Ks; range 0–105) [3]. -
Apoptosis Ligand-Induced Enhanced Resistance to Fas/Fas
Theileria parva-Transformed T Cells Show Enhanced Resistance to Fas/Fas Ligand-Induced Apoptosis This information is current as Peter Küenzi, Pascal Schneider and Dirk A. E. Dobbelaere of October 2, 2021. J Immunol 2003; 171:1224-1231; ; doi: 10.4049/jimmunol.171.3.1224 http://www.jimmunol.org/content/171/3/1224 Downloaded from References This article cites 69 articles, 29 of which you can access for free at: http://www.jimmunol.org/content/171/3/1224.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on October 2, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2003 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Theileria parva-Transformed T Cells Show Enhanced Resistance to Fas/Fas Ligand-Induced Apoptosis1 Peter Ku¨enzi,2* Pascal Schneider,† and Dirk A. E. Dobbelaere3* Lymphocyte homeostasis is regulated by mechanisms that control lymphocyte proliferation and apoptosis. Activation-induced cell death is mediated by the expression of death ligands and receptors, which, when triggered, activate an apoptotic cascade.