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  • 1
    Online Resource
    Online Resource
    Hauppauge :Nova Science Publishers, Incorporated,
    Keywords: Electroporation. ; Electroporation -- Therapeutic use. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (352 pages)
    Edition: 1st ed.
    ISBN: 9781616683832
    Series Statement: None
    DDC: 571.6/4
    Language: English
    Note: Intro -- ELECTROPORATION IN LABORATORY AND CLINICAL INVESTIGATIONS -- ELECTROPORATION IN LABORATORY AND CLINICAL INVESTIGATIONS -- CONTENTS -- PREFACE -- Chapter 1 MATHEMATICAL-PHYSICAL MODELING AND BIOMEDICAL OPTIMIZATION OF CELL ELECTROPERMEABILIZATION: AN OVERVIEW -- ABSTRACT -- INTRODUCTION -- I. ARE THERE ALTERNATIVE MODELS OF ELECTROPERMEABILIZATION? -- II. PHYSICS OF ELECTROPORATION FROM THE GENERAL AND KINETIC STANDPOINTS -- III. MATHEMATICAL MODELING OF ELECTROPORE NUCLEATION AND EVOLUTION -- IV. A DIRECT VIEW ON ELECTROPORE FORMATION: THE PERSPECTIVE OF MOLECULAR SIMULATIONS -- V. THE IN VIVO SETTING -- CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES -- Chapter 2 TECHNICAL ASPECTS OF THE ELECTROCHEMOTHERAPY -- ELECTROPORATION. SHORT DESCRIPTION OF THE PHENOMENON. TRANSMEMBRANE VOLTAGE INDUCED BY ELECTRIC FIELD ON ISOLATED CELL -- TECHNIQUES FOR INDUCING THE ELECTRIC FIELD -- ELECTROPORATION IN CELL SUSPENSION AND TISSUES -- ELECTROCHEMOTHERAPY. ELECTROGENETRANSFECTION -- OPTIMIZATION OF THE PULSE PARAMETERS -- ELECTRODES -- GENERATORS -- RISK OF FIBRILLATION -- OUR OWN STUDIES AND INSTRUMENT DESIGN -- REFERENCES -- Chapter 3 NON-THERMAL IRREVERSIBLE ELECTROPORATION FOR TISSUE ABLATION -- ABSTRACT -- INTRODUCTION -- IRREVERSIBLE ELECTROPORATION FOR NON-THERMAL TISSUE ABLATION -- HISTORY -- THEORY OF IRREVERSIBLE ELECTROPORATION -- NUMERICAL MODELING FOR TREATMENT PLANNING -- Models: -- Electric Field Distribution -- Joule Heating -- COMMON PHYSICAL PROPERTIES: -- Temperature Distribution: -- Equivalent Thermal Dose -- Thermal Damage Equation: -- SPECIAL CONSIDERATIONS -- Heterogeneous Tissue: -- Dynamic Properties During Electroporation -- Temperature Dependent Properties -- CONCLUSION -- REFERENCES -- Chapter 4 MECHANISMS OF MICROORGANISM INACTIVATION BY PULSED ELECTRIC FIELDS -- ABSTRACT -- INTRODUCTION -- THEORY. , COMPARISON WITH EXPERIMENTS AND DISCUSSION -- ACKNOWLEDGMENT -- REFERENCES -- Chapter 5 ELECTROCHEMICAL PROCESSES OCCURING DURING CELL ELECTROMANIPULATION PROCEDURES -- ABSTRACT -- INTRODUCTION -- THEORETICAL BACKGROUND -- Primary Cathodic Half-Reactions -- Primary Anodic Half-Reactions -- Secondary Chemical Reactions -- CONSEQUENCES OF ELECTROCHEMICAL PROCESSES -- Consequences of Cathodic Processes -- Consequences of Anodic Processes -- Consequences of Secondary Chemical Reactions -- CONCLUSION -- ACKNOWLEDGMENT -- REFERENCES -- Chapter 6 ULTRASTRUCTURAL MODIFICATIONS INDUCED BY "ELECTROPORATION" -- ABSTRACT -- INTRODUCTION -- ELECTROPORATION FOR TRANSDERMAL DRUG DELIVERY -- ELECTROPORATION ON MELANOMA XENOGRAFTS -- CONCLUSION -- ACKNOWLEDGMENT -- REFERENCES -- Chapter 7 ELECTROPORATION IN BACTERIA -- ABSTRACT -- INTRODUCTION -- KEY STEPS PRIOR TO ELECTROPORATION -- Preparation of Electrocompetent Cells -- Growth Stage and Concentration of Cells -- Growth Medium Composition and Growth Temperature -- Size, Form, and Concentration of DNA -- Electroporation Buffers and Timing of Plasmid Addition -- ELECTROPORATION CONDITIONS -- Pulsed Electric Field Application -- Electrical Parameters and The Technology of Electroporation -- Post-Pulse Treatments -- EXAMPLES OF APPLICATIONS -- Escherichia Coli -- Preparation of Electrocompetent Cells -- Electroporation -- Lactococcus lactis -- Preparation of Electrocompetent Cells -- Electroporation -- REFERENCES -- Chapter 8 ELECTROPORATION OF PLANT CELLS -- ABSTRACT -- INTRODUCTION -- ELECTROPORATION OF PROTOPLASTS -- ELECTROPORATION OF INTACT PLANT CELLS AND TISSUES -- ELECTROPORATION CONDITIONS -- ELECTROPORATION OF PLANT ORGANELLES -- Chloroplasts -- Mitochondrion -- CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES. , Chapter 9 ANTI-TUMORAL EFFECTS OF PULSED LOW ELECTRIC FIELD ENHANCED CHEMOTHERAPY: LESSONS FROM EXPERIMENTAL MALIGNANT TUMORS -- ABSTRACT -- 1. INTRODUCTION -- 1.1. Enhancement of the Uptake of Molecules and Macromolecules by Cells -- 1.2. Enhanced Uptake of Molecules and Macromolecules by Non-Permeabilizing Unipolar Pulsed Low Electric Fields (LEF) -- 1.3. The Difference between Enhanced Uptake of Molecules Induced by Electroporation and by Unipolar Pulsed Train of Low Electric Fields (LEF) -- 1.4. Application of Electric Based Cancer Therapy -- 1.4.1. Electrotherapy by Low Intensity DC Electric-Fields (LIEF) -- 1.4.2. Electrochemotherapy by High Electric Fields (ECT) -- 1.4.3. Electrotherapy by High Frequency Electric Fields -- 1.4.4. Electro-Hyperthermia -- 2. ANTI-TUMORAL EFFECTS OF LOW ELECTRIC FIELD CANCER TREATMENT-ENHANCED CHEMOTHERAPY (LEFCT-EC) -- 2.1. Experimental Design And Methods: -- 2.1.1. Experimental Metastatic Tumors -- 2.1.2. Chemotherapy -- 2.1.3. Low Electric Field Cancer Therapy Protocol -- 2.2. Treatment of Mouse Melanoma Derived Tumors by LEFCT-EC -- 2.3. Treatment of Mouse Mammary Carcinoma Derived Tumors by LEFCT-EC -- 2.4. Effective Treatment of Mouse Metastatic Squamous Cell Carcinoma (SCC) Cancer by Low Electric Fields and Chemotherapy -- 2.5. Effective Treatment of Mouse Metastatic Prostate Cancer by Low Electric Fields and Chemotherapy -- 2.6. Cure of Primary Colon Cancer Derived Tumors and Reduction in the Metastatic Load Following LEFCT-EC -- 2.6.1. The Role of the Electric Pulse Intensity -- 2.6.2.The Combination of the Electric Stimulus with Different Chemotherapeutic Drugs. -- 2.6.3. The Ability of LEFCT-EC to Control Primary as Well as Metastatic Disease -- 3. THE INVOLVEMENT OF IMMUNOLOGICAL COMPONENTS IN THE ARREST OF METASTATIC GROWTH ACHIEVED BY DESTRUCTION OF THE PRIMARY TUMOR BY LEFCT AND LEFCT-EC. , 3.1. The Development of an Anti Tumoral Reaction Following LEFCT-EC of B16 Melanoma -- 3.2. Breast Cancer Cell (DA3) Tumor Destruction By LEFCT And LEFCT-EC Triggered Anti Tumor Reaction -- 3.3. SCC Tumor (SQ2) Destruction by LEFCT and LEFCT-EC and Anti Tumor Reaction -- 3.4. Anti Tumor Immunity Against Prostate Cancer Cell Tumors (TRAMP) Following Destruction of the Tumors by LEFCT-EC -- 3.5. Involvement of the Immune Response in the Cure of Metastatic Murine CT-26 Colon Carcinoma by LEFCT-EC -- 3.6 Induction of Anti-Tumor Immunity by other Ablation Mechanisms, Which Cause in Situ Tumor Ablation -- CONCLUSION -- REFERENCES -- Chapter 10 ELECTROGENETHERAPY: ELECTROGENE TRANSFER USING LOW FIELD STRENGTH -- ABSTRACT -- INTRODUCTION -- A NOVEL SYRINGE ELECTRODE USES AMUCH LOWER ELECTRIC FIELD STRENGTH THAN CONVENTIONAL ELECTRODES -- ELECTROPHORESIS ACROSS THE PLASMA MEMBRANE MAY NOT BE INVOLOVED IN IN VIVO DNA TRANSPORT -- THE FIELD STRENGTH FOR ELECTROGENE TRANSFER CAN BE FURTHER REDUCED USING SINE-WAVE CURRENT PULSES -- CONCLUSION -- REFERENCES -- Chapter 11 ELECTROPORATION - TREATING MICE OR MEN? -- ABSTRACT -- INTRODUCTION -- ANIMAL MODELS IN PRECLINICAL STUDIES -- Anemia -- Arthritis -- Diabetes -- Ocular Disease -- Multiple Sclerosis -- Growth Hormone-Releasing Hormone -- Other Studies -- DELIVERY OF DNA VACCINES WITH ELECTROPORATION -- CLINICAL STUDIES -- CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES -- Chapter 12 ELECTROCHEMOTHERAPY IN VETERINARY MEDICINE, PART I: SOLID TUMORS -- ABSTRACT -- PRELIMINARY STUDIES AND FIRST PROTOCOLS -- ELECTROCHEMOTHERAPY FOR SPECIFIC TUMOR TYPES: PHASE II STUDIES -- REFERENCES -- Chapter 13 ELECTROCHEMOTHERAPY IN VETERINARY MEDICINE, PART II: ROUND CELL TUMORS -- ABSTRACT -- PRELIMINARY STUDIES AND FIRST PROTOCOLS -- ELECTROCHEMOTHERAPY FOR SPECIFIC TUMOR TYPES: PHASE II STUDIES -- CONCLUSIONS -- REFERENCES. , Chapter 14 HISTOPATHOLOGICAL ANALYSIS OF CANINE AND FELINE CANCER TREATED WITH ELECTROCHEMOTHERAPY -- ABSTRACT -- MATERIAL AND METHODS -- RESULTS -- DISCUSSION -- REFERENCES -- Chapter 15 CLINICAL APPLICATION OF ELECTROCHEMOTHERAPY - AN ADJUNCT TO SURGERY -- 1. INTRODUCTION -- 2. SYSTEMS AND ELECTRODES EMPLOYED FOR CLINICAL APPLICATION -- 3. APPROPRIATE DRUGS FOR ELECTROCHEMOTHERAPY -- 3.1. Bleomycin -- 3.1.1. Indications -- 3.1.2. Mechanism of Action -- 3.1.3. Clinical Drug Dosage -- 3.1.4. Route of Administration and Timing -- 3.1.5. Toxicity and Side Effects -- 3.2. Cisplatin -- 3.2.1 .Indications -- 3.2.2. Mechanism of Action -- 3.2.3. Drug Dosage -- 3.2.4. Route of Administration and Timing -- 3.2.5. Toxicity and Side Effects -- 4. TREATMENT PROTOCOL -- 4.1. Eligibility Criteria -- 4.2. Anaesthesia -- 4.3. Patient Follow-Up -- 4.4. Response Criteria -- 5. EARLY CLINICAL EXPERIENCE -- 5.1. Clinical Trials Involving Bleomycin -- 5.2. Clinical Trials Involving Cisplatin -- 6. ESOPE TRIAL (TAKEN FROM [20]) -- 6.1. Background -- 6.2. Patient Population -- 6.3. Tumour Histologies -- 6.4. Overall Response -- 6.5. Influence of Drug Delivery -- 6.6. Influence of Tumour Locale -- 6.7. Influence of Tumour Volume -- 6.8. Influence of Electrode Type -- 7. LIMITATIONS OF ELECTROCHEMOTHERAPY -- 7.1. Side Effects Related to Therapy -- 7.2. Patient Referral Criteria -- 7.3. Limitation of Clinical Utility -- 7.4. Need for Comparison Studies with other Therapeutic Modalities -- 8. DEVELOPMENTAL PERSPECTIVES -- 8.1. Extension of Clinical Utility -- 8.2. Enhancement of Existing Therapeutic Regimens -- 8.3. Gene Delivery Vector -- 8.4. Microneedles -- 8.5. Nanoparticles -- CONCLUSIONS -- REFERENCES -- Chapter 16 ELECTROPORATION IN CHRONIC LYMPHOCYTIC LEUKEMIA -- ABSTRACT -- INTRODUCTION -- Chronic Lymphocytic Leukemia. , Opportunities for Gene Transfer in CLL Research.
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  • 2
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: APAF-1 plays a pivotal role in mitochondria-dependent apoptosis, binding to cytochrome c and favoring activation of caspase-9. It has been shown that epigenetic silencing of the APAF-1 gene is a common event in several metastatic melanoma cells in vitro. We determined, by Western blot, variation in the level of expression of APAF-1 in several human melanoma cell lines and, by immunohistochemistry, in a group of 106 histological samples including benign and malignant melanocytic lesions. We observed APAF-1 down-regulation or loss of expression in two metastatic melanoma cell lines, compared to primary melanoma cell lines. The immunohistochemical analysis revealed a significant difference in APAF-1 staining between nevi and melanomas. In addition, we found a significant negative correlation between APAF-1 expression level and tumor thickness and between primary melanomas and metastases. We conclude that loss of APAF-1 expression can be considered as an indicator of malignant transformation in melanoma.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In order to identify genes relevant for melanoma development, we carried out cDNA array experiments employing an in vitro model of human melanoma progression, consisting of two cell lines: one, LP, derived from a primary melanoma and the other, LM, from its metastatic supraclavicular lymph node. Basic cDNA array data identified 26 genes as down-regulated in the LM cell line. Northern blot analysis confirmed an effective transcriptional down-regulation for five out of 13 genes analyzed. The products of these five genes belong to different functional protein types, such as transcription and translation regulators (Edg-2, eIF-3 p110, and RNPL/RBM3), extracellular communicators (PRSS11) and members of the major histocompatibility complex (β2-microglobulin). Some previously described differences in expression patterns, such as loss of HLA I, were confirmed by our array data. In addition, we identified and validated for the first time the reduced expression level of several genes during melanoma progression. In particular, reduced Edg-2 gene product expression was also confirmed in a group of 50 primary melanomas and unrelated metastases. In conclusion, comparative hybridization by means of cDNA arrays assisted in identifying a series of novel progression-associated changes in gene expression, confirming, at the same time, a number of previously described results.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 10 (1998), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It has been known for a long time that subcortical input drives the specification of cortical areas. Molecular signals mediating this instructive effect from the periphery are poorly understood. In foetal or neonatal rats, ablation of whisker follicles, transection of the infraorbital nerve, inhibition of axonal transport, but not impulse activity blockade, prevent formation of barrels in the primary somatosensory cortex (S1). These findings suggest that a chemical signal, possibly arising from the skin or the follicle, may be responsible for somatotopic pattern formation in S1. Neurotrophins promote survival and differentiation of primary sensory neurons, and are expressed in the whisker pad during development. Neonatal rats received gelfoam impregnated with NGF, BDNF or NT-3 under the whisker pad following surgical denervation of whisker rows D and E on P0. Barrel formation in S1 was assessed on P7 by acetylcholinesterase histochemistry and 5-HT-immunohistochemistry. BDNF and NT-3, but not NGF, promoted development of the cortical barrels corresponding to denervated whiskers. Furthermore, BDNF and NT-3 prevented the lesion-induced expansion of row C barrels, while NGF appeared to promote row C expansion. Our results suggest that BDNF and NT-3 arising from the whisker pad are involved in the formation and/or maintenance of the barrel pattern in S1. These findings are potentially relevant for the prevention of sensory disturbances possibly due to reorganization of central sensory circuits after peripheral nerve lesions in humans.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: This study shows that unilateral transection of the infraorbital nerve (ION) in newborn (P0) rats induces apoptosis in the contralateral ventrobasal thalamic (VB) complex, as evidenced by terminal transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL) and electron miscroscopy. Double-labelling experiments using retrograde transport of labelled microspheres injected into the barrel cortex, followed by TUNEL staining, show that TUNEL-positive cells are thalamocortical neurons. The number of TUNEL-positive cells had begun to increase by 24 h postlesion, increased further 48 h after nerve section, and decreased to control levels after 120 h. Lesion-induced apoptosis in the VB complex is less pronounced if ION section is performed at P4, and disappears if the lesion is performed at P7. This time course closely matches the critical period of lesion-induced plasticity in the barrel cortex. Nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF), applied on the ION stump alone or in combination, are able to partially rescue thalamic neurons from apoptosis. Total cell counts in the VB complex of P7 animals that underwent ION section at P0 confirm the rescuing effect of BDNF and NGF. Blockade of axonal transport in the ION mimics the effect of ION section. These data suggest that survival-promoting signals from the periphery, maybe neurotrophins, are required for the survival of higher-order neurons in the somatosensory system during the period of fine-tuning of neuronal connections. We also propose that anterograde transneuronal degeneration in the neonatal rat trigeminal system may represent a new animal model for studying the pathways of programmed cell death in vivo.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    International journal of dermatology 42 (2003), S. 0 
    ISSN: 1365-4632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A 24-year-old woman was seen in consultation for a painless tumor of 6 cm in diameter of the vulva. The excised oval tumor was situated in the lower part of the dermis and encapsulated (〈link href="#f1"〉Fig. 1A). It was completely composed of multiple adjacent cell complexes, each containing 5–20 laminar cells and resembling Wagner–Meissner touch corpuscles (〈link href="#f1"〉Fig 1B and 1C). The nuclei of the laminar cells were located at the periphery of the corpuscles or were arranged transversely to the long axis of these structures along the lamellae. The nuclei were oval or showed one or several nuclear invaginations. Mitoses were not observed. These corpuscles showed a positive immunohistochemical reaction for S-100 (〈link href="#f1"〉Fig. 1D), vimentin, and neuron-specific endase (NSE) (not shown), but were negative for CD-68, desmin, and α-actin. The gross and microscopic morphology and the immunohistochemical findings were compatible with a diagnosis of Wagner–Meissner neurilemmoma of the vulva. The patient remained disease free for 2 years after surgery.〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD1756_1:IJD_1756_f1"/〉(A) Gross appearance of the excised oval tumor of the vulva, situated in the lower part of the dermis and encapsulated. (B) Histologic examination of the excised lesion revealed a monomorphous morphology with typical touch corpuscles with lamellar structures (hematoxylin and eosin; original magnification, × 50). (C) Higher magnification of (B). The nuclei are predominantly located at the periphery of the corpuscles (hematoxylin and eosin; original magnification, × 250). (D) The tactile corpuscles show a positive reaction for protein S-100 (3-amino-9-ethylcarbazide, × 250)
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK; Malden, USA : Munksgaard International Publishers
    Experimental dermatology 14 (2005), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  Apoptosis protease-activating factor-1 (Apaf-1) is a key regulator of the mitochondrial apoptotic pathway, being the central element of the multimeric apoptosome formed by procaspase 9, cytochrome c, and Apaf-1 itself. In this review, the principal aspects about Apaf-1 gene structure and function, and its role in the apoptotic machinery, are described. Moreover, the most recent findings about the involvement of this molecule in melanoma progression and chemoresistance, as well as the clinico-pathological relevance of these findings in the treatment of this deadly disease, are reported.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Bardet–Biedl syndrome (BBS, MIM 209900) is a heterogeneous autosomal recessive disorder characterized by obesity, pigmentary retinopathy, polydactyly, renal malformations, mental retardation, and hypogenitalism. The disorder is also associated with diabetes mellitus, hypertension, and ...
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The oncoprotein of simian virus-40, SV40 large T-antigen (Tag), is reported to target and to inactivate growth suppressive proteins such as the retinoblastoma family1–3 and p53 (ref. 4, 5), leading to transformation of human cell lines in vitro, tumor production in rodents6, and detection of ...
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0730-2312
    Keywords: tumor suppressor gene ; retinoblastoma gene ; Rb2/p130 ; pocket protein ; nuclear phosphoprotein ; E1A oncoprotein ; cell cycle ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The Rb2/p130 protein has been shown to have a high sequence homology with the retinoblastoma gene product (pRb), one of the most well-characterized tumor suppressor genes, and with pRb-related p107, especially in their conserved pocket domains, which display a primary role in the function of these proteins. In this study, we report on the biochemical and immunocytochemical characterization of the Rb2/p130 protein, using a polyclonal antibody developed against its “spacer” region included in the pocket domain of the whole protein. We show that pRb/p130 is a phosphoprotein located at the nuclear level and that its phosphorylation pathway can be dramatically reduced by phosphatase treatment. Moreover pRb/p130, with p107, with p107, is one of the major targets of the E1A viral oncoprotein-associated kinase activity, showing a phosphorylation pattern which is modulated during the cell cycle, reaching a peak of activation at the onset of S-phase. © 1995 Wiley-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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