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Book: A National Institutes of Health lecture entitled "Inositol lipids and intracellular communication" by Michael J. Berridge, Ph. D., September 23, 1987

Berridge, Michael J

1987

Title variant	Inositol lipids and intracellular communication
Institution	National Institutes of Health (U.S.)
MeSH term(s)	Inositol Phosphates ; Cell Communication/drug effects ; Phospholipids/metabolism ; Sugar Phosphates/metabolism
Language	English
Size	1 videocassette :, sd., col. ;, 3/4 in.
Publisher	National Institutes of Health
Publishing place	Bethesda, Md
Document type	Book
Note	Title from cassette label.
Database	Catalogue of the US National Library of Medicine (NLM)

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Article: Lymphocyte Activation in Health and Disease.

Berridge, Michael J

Critical reviews in immunology

2018 Volume 37, Issue 2-6, Page(s) 439–462

Abstract: Lymphocytes employ a complex assembly of signaling elements that have been organized on a spatiotemporal map to define their role in stimulating both proliferation and apoptosis. The antigen/major histocompatibility complex (MHC) initiates the sequence ... ...

Abstract	Lymphocytes employ a complex assembly of signaling elements that have been organized on a spatiotemporal map to define their role in stimulating both proliferation and apoptosis. The antigen/major histocompatibility complex (MHC) initiates the sequence by organizing the assembly of an active T-cell receptor (TCR) complex responsible for transmitting information down various signaling cassettes (e.g., the IP3/Ca2+, DAG/ PKC, ras/MAPK, and the PI 3-K pathways). It is proposed that CD28 may exert its costimulatory action by facilitating the assembly of an effective scaffold of signaling elements within the TCR complex. The absence of costimulation through CD28 seems to result in the assembly of a defective scaffold that reverses slowly and may thus account for the state of unresponsiveness responsible for peripheral T-cell tolerance. The signaling cassettes activated by the TCR and CD28 then engage cytosolic factors that transmit information into the nucleus to activate the genes that code for the IL-2 and Fas signaling pathways. The IL-2 and Fas receptors employ additional signaling cassettes (e.g., the JAK/STAT and the sphingomyelinase/ceramide pathways) to mediate their effects on proliferation and apoptosis, respectively. Information concerning these signaling systems is beginning to provide therapeutic strategies to manipulate the immune system to overcome human immunodeficiency virus (HIV) infection, autoimmune diseases, and graft rejection.
MeSH term(s)	Apoptosis/immunology ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/immunology ; B-Lymphocytes/drug effects ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; CD28 Antigens/immunology ; CD28 Antigens/metabolism ; Cell Proliferation ; Graft Rejection/drug therapy ; Graft Rejection/immunology ; HIV Infections/drug therapy ; HIV Infections/immunology ; Humans ; Immune Tolerance/drug effects ; Immune Tolerance/immunology ; Immunosuppressive Agents/pharmacology ; Immunosuppressive Agents/therapeutic use ; Interleukin-2/immunology ; Interleukin-2/metabolism ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Major Histocompatibility Complex/immunology ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Interleukin-2/immunology ; Receptors, Interleukin-2/metabolism ; Signal Transduction/drug effects ; Signal Transduction/immunology ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; fas Receptor/immunology ; fas Receptor/metabolism
Chemical Substances	CD28 Antigens ; Immunosuppressive Agents ; Interleukin-2 ; Receptors, Antigen, T-Cell ; Receptors, Interleukin-2 ; fas Receptor
Language	English
Publishing date	2018-06-19
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1353116-5
ISSN	1040-8401
ISSN	1040-8401
DOI	10.1615/CritRevImmunol.v37.i2-6.120
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Article ; Online: Calcium signalling in health and disease.

Berridge, Michael J

Biochemical and biophysical research communications

2017 Volume 485, Issue 1, Page(s) 5

Language	English
Publishing date	2017-03-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2017.01.098
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Article ; Online: Vitamin D and Depression: Cellular and Regulatory Mechanisms.

Berridge, Michael J

Pharmacological reviews

2017 Volume 69, Issue 2, Page(s) 80–92

Abstract: Depression is caused by a change in neural activity resulting from an increase in glutamate that drives excitatory neurons and may be responsible for the decline in the activity and number of the GABAergic inhibitory neurons. This imbalance between the ... ...

Abstract	Depression is caused by a change in neural activity resulting from an increase in glutamate that drives excitatory neurons and may be responsible for the decline in the activity and number of the GABAergic inhibitory neurons. This imbalance between the excitatory and inhibitory neurons may contribute to the onset of depression. At the cellular level there is an increase in the concentration of intracellular Ca
MeSH term(s)	Alzheimer Disease/metabolism ; Animals ; Calcium Signaling ; Depression/metabolism ; Depression/physiopathology ; Humans ; Inflammation/metabolism ; Inflammation/physiopathology ; Neurons/physiology ; Vitamin D/metabolism
Chemical Substances	Vitamin D (1406-16-2)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209898-2
ISSN	1521-0081 ; 0031-6997
ISSN (online)	1521-0081
ISSN	0031-6997
DOI	10.1124/pr.116.013227
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Article ; Online: Vitamin D deficiency accelerates ageing and age-related diseases: a novel hypothesis.

Berridge, Michael J

The Journal of physiology

2017 Volume 595, Issue 22, Page(s) 6825–6836

Abstract: Ageing can occur at different rates, but what controls this variable rate is unknown. Here I have developed a hypothesis that vitamin D may act to control the rate of ageing. The basis of this hypothesis emerged from studyng the various cellular ... ...

Abstract	Ageing can occur at different rates, but what controls this variable rate is unknown. Here I have developed a hypothesis that vitamin D may act to control the rate of ageing. The basis of this hypothesis emerged from studyng the various cellular processes that control ageing. These processes such as autophagy, mitochondrial dysfunction, inflammation, oxidative stress, epigenetic changes, DNA disorders and alterations in Ca
MeSH term(s)	Aging/metabolism ; Aging/pathology ; Aging/physiology ; Animals ; Calcium Signaling ; Cellular Senescence ; Humans ; Neurodegenerative Diseases/etiology ; Oxidative Stress ; Vitamin D Deficiency/complications ; Vitamin D Deficiency/metabolism ; Vitamin D Deficiency/physiopathology
Language	English
Publishing date	2017-10-31
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP274887
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Article ; Online: Vitamin D deficiency and diabetes.

Berridge, Michael J

The Biochemical journal

2017 Volume 474, Issue 8, Page(s) 1321–1332

Abstract: Vitamin D deficiency has been linked to the onset of diabetes. This review summarizes the role of Vitamin D in maintaining the normal release of insulin by the pancreatic beta cells (β-cells). Diabetes is initiated by the onset of insulin resistance. The ...

Abstract	Vitamin D deficiency has been linked to the onset of diabetes. This review summarizes the role of Vitamin D in maintaining the normal release of insulin by the pancreatic beta cells (β-cells). Diabetes is initiated by the onset of insulin resistance. The β-cells can overcome this resistance by releasing more insulin, thus preventing hyperglycaemia. However, as this hyperactivity increases, the β-cells experience excessive Ca
MeSH term(s)	Animals ; Apoptosis ; Calcium Signaling ; DNA Methylation ; Diabetes Mellitus, Type 1/etiology ; Diabetes Mellitus, Type 1/prevention & control ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/prevention & control ; Dietary Supplements ; Epigenesis, Genetic ; Evidence-Based Medicine ; Humans ; Insulin/metabolism ; Insulin Resistance ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Oxidative Stress ; Vitamin D/therapeutic use ; Vitamin D Deficiency/diet therapy ; Vitamin D Deficiency/metabolism ; Vitamin D Deficiency/pathology ; Vitamin D Deficiency/physiopathology
Chemical Substances	Insulin ; Vitamin D (1406-16-2)
Language	English
Publishing date	2017-03-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20170042
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Article ; Online: Vitamin D deficiency: infertility and neurodevelopmental diseases (attention deficit hyperactivity disorder, autism, and schizophrenia).

Berridge, Michael J

American journal of physiology. Cell physiology

2017 Volume 314, Issue 2, Page(s) C135–C151

Abstract: The process of development depends on a number of signaling systems that regulates the progressive sequence of developmental events. Infertility and neurodevelopmental diseases, such as attention deficit hyperactivity disorder, autism spectrum disorders, ...

Abstract	The process of development depends on a number of signaling systems that regulates the progressive sequence of developmental events. Infertility and neurodevelopmental diseases, such as attention deficit hyperactivity disorder, autism spectrum disorders, and schizophrenia, are caused by specific alterations in these signaling processes. Calcium signaling plays a prominent role throughout development beginning at fertilization and continuing through early development, implantation, and organ differentiation such as heart and brain development. Vitamin D plays a major role in regulating these signaling processes that control development. There is an increase in infertility and an onset of neurodevelopmental diseases when vitamin D is deficient. The way in which vitamin D deficiency acts to alter development is a major feature of this review. One of the primary functions of vitamin D is to maintain the phenotypic stability of both the Ca
MeSH term(s)	Animals ; Attention Deficit Disorder with Hyperactivity/epidemiology ; Attention Deficit Disorder with Hyperactivity/metabolism ; Attention Deficit Disorder with Hyperactivity/physiopathology ; Attention Deficit Disorder with Hyperactivity/psychology ; Autistic Disorder/epidemiology ; Autistic Disorder/metabolism ; Autistic Disorder/physiopathology ; Autistic Disorder/psychology ; Brain/metabolism ; Brain/physiopathology ; Calcium Signaling ; Fertility ; Humans ; Infertility/epidemiology ; Infertility/metabolism ; Infertility/physiopathology ; Risk Factors ; Schizophrenia/epidemiology ; Schizophrenia/metabolism ; Schizophrenia/physiopathology ; Schizophrenic Psychology ; Vitamin D/metabolism ; Vitamin D Deficiency/epidemiology ; Vitamin D Deficiency/metabolism
Chemical Substances	Vitamin D (1406-16-2)
Language	English
Publishing date	2017-10-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00188.2017
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Article ; Online: The Inositol Trisphosphate/Calcium Signaling Pathway in Health and Disease.

Berridge, Michael J

Physiological reviews

2016 Volume 96, Issue 4, Page(s) 1261–1296

Abstract: Many cellular functions are regulated by calcium (Ca(2+)) signals that are generated by different signaling pathways. One of these is the inositol 1,4,5-trisphosphate/calcium (InsP3/Ca(2+)) signaling pathway that operates through either primary or ... ...

Abstract	Many cellular functions are regulated by calcium (Ca(2+)) signals that are generated by different signaling pathways. One of these is the inositol 1,4,5-trisphosphate/calcium (InsP3/Ca(2+)) signaling pathway that operates through either primary or modulatory mechanisms. In its primary role, it generates the Ca(2+) that acts directly to control processes such as metabolism, secretion, fertilization, proliferation, and smooth muscle contraction. Its modulatory role occurs in excitable cells where it modulates the primary Ca(2+) signal generated by the entry of Ca(2+) through voltage-operated channels that releases Ca(2+) from ryanodine receptors (RYRs) on the internal stores. In carrying out this modulatory role, the InsP3/Ca(2+) signaling pathway induces subtle changes in the generation and function of the voltage-dependent primary Ca(2+) signal. Changes in the nature of both the primary and modulatory roles of InsP3/Ca(2+) signaling are a contributory factor responsible for the onset of a large number human diseases.
MeSH term(s)	Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling/physiology ; Humans ; Inositol 1,4,5-Trisphosphate/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism ; Signal Transduction/physiology
Chemical Substances	Calcium Channels ; Ryanodine Receptor Calcium Release Channel ; Inositol 1,4,5-Trisphosphate (85166-31-0) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00006.2016
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Article ; Online: Vitamin D, reactive oxygen species and calcium signalling in ageing and disease.

Berridge, Michael J

Philosophical transactions of the Royal Society of London. Series B, Biological sciences

2016 Volume 371, Issue 1700

Abstract: Vitamin D is a hormone that maintains healthy cells. It functions by regulating the low resting levels of cell signalling components such as Ca(2+) and reactive oxygen species (ROS). Its role in maintaining phenotypic stability of these signalling ... ...

Abstract	Vitamin D is a hormone that maintains healthy cells. It functions by regulating the low resting levels of cell signalling components such as Ca(2+) and reactive oxygen species (ROS). Its role in maintaining phenotypic stability of these signalling pathways depends on the ability of vitamin D to control the expression of those components that act to reduce the levels of both Ca(2+) and ROS. This regulatory role of vitamin D is supported by both Klotho and Nrf2. A decline in the vitamin D/Klotho/Nrf2 regulatory network may enhance the ageing process, and this is well illustrated by the age-related decline in cognition in rats that can be reversed by administering vitamin D. A deficiency in vitamin D has also been linked to two of the major diseases in man: heart disease and Alzheimer's disease (AD). In cardiac cells, this deficiency alters the Ca(2+) transients to activate the gene transcriptional events leading to cardiac hypertrophy and the failing heart. In the case of AD, it is argued that vitamin D deficiency results in the Ca(2+) landscape that initiates amyloid formation, which then elevates the resting level of Ca(2+) to drive the memory loss that progresses to neuronal cell death and dementia.This article is part of the themed issue 'Evolution brings Ca(2+) and ATP together to control life and death'.
MeSH term(s)	Aging ; Alzheimer Disease/metabolism ; Animals ; Calcium/metabolism ; Calcium Signaling ; Heart Diseases/metabolism ; Humans ; Mice ; Rats ; Reactive Oxygen Species/metabolism ; Vitamin D/metabolism
Chemical Substances	Reactive Oxygen Species ; Vitamin D (1406-16-2) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2016-08-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208382-6
ISSN	1471-2970 ; 0080-4622 ; 0264-3839 ; 0962-8436
ISSN (online)	1471-2970
ISSN	0080-4622 ; 0264-3839 ; 0962-8436
DOI	10.1098/rstb.2015.0434
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Article ; Online: Vitamin D: a custodian of cell signalling stability in health and disease.

Berridge, Michael J

Biochemical Society transactions

2015 Volume 43, Issue 3, Page(s) 349–358

Abstract: There is increasing evidence that a deficiency in vitamin D contributes to many human diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), hypertension and cardiovascular disease. The ability of vitamin D to ... ...

Abstract	There is increasing evidence that a deficiency in vitamin D contributes to many human diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), hypertension and cardiovascular disease. The ability of vitamin D to maintain healthy cells seems to depend on its role as a guardian of phenotypic stability particularly with regard to the reactive oxygen species (ROS) and Ca2+ signalling systems. Vitamin D maintains the expression of those signalling components responsible for stabilizing the low-resting state of these two signalling pathways. This vitamin D signalling stability hypothesis proposes that vitamin D, working in conjunction with klotho and Nrf2 (nuclear factor-erythroid-2-related factor 2), acts as a custodian to maintain the normal function of the ROS and Ca2+ signalling pathways. A decline in vitamin D levels will lead to an erosion of this signalling stability and may account for why so many of the major diseases in man, which have been linked to vitamin D deficiency, are associated with a dysregulation in both ROS and Ca2+ signalling.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Calcium Signaling/genetics ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Humans ; Multiple Sclerosis/genetics ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Reactive Oxygen Species/metabolism ; Vitamin D/genetics ; Vitamin D/metabolism
Chemical Substances	NF-E2-Related Factor 2 ; NFE2L2 protein, human ; Reactive Oxygen Species ; Vitamin D (1406-16-2) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2015-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20140279
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