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Michael Berridge retired from his position as Head of Cell Signalling at Babraham in 2003. He continues to work at Babraham as an Emeritus Babraham Fellow. He retains his interest in cell signalling by writing and maintaining a website (www.cellsignallingbiology.org) which is hosted by Portland Press. The primary aim of this website is to describe cell signalling within its normal biological context. The beauty of cell signalling is the way different pathways are combined and adapted to control a diverse array of cellular process in widely different spatial and temporal domains. The emerging information on cell signalling pathways is integrated and presented within the context of specific cell types and processes. This intimate relationship between cell signalling and biology is providing valuable insights into the underlying genetic and phenotypic defects responsible for many of the major human diseases.
I was born in 1938 in a small town called Gatooma in Southern Rhodesia. This country in central Africa has changed its names several times; it became Rhodesia and more recently Zimbabwe. My earliest memories are of Eiffel Flats, a small gold mining town about five miles from Kadoma. It was in the heart of the African bush with its rich variety of animals and birds, which excited me as a young boy and has continued to fascinate me ever since. My love of nature inspired my initial interest in academic studies. While at school, I spent some of my spare time writing notes and drawing pictures of the animals that surrounded me and these early experiences of life in Africa shaped my scientific career.
A drawing of kudu from my schoolboy notebook
on African wild animals (click to enlarge)
While at school, I was fortunate in being taught biology by Pamela Bates who not only fostered my academic interests but also opened my eyes to the fact that there was an academic life after school.
Miss Bates gave me the confidence and inspiration to pursue an academic career and helped me to apply for a place at the newly founded University of Rhodesia and Nyasaland in Salisbury to read Zoology and Chemistry. During my early courses I was intent on moving into the field of big game ecology. However, my interest began to change following the physiology lectures given by Dr Eina Bursell an insect physiologist.
Pamela Bates and Michael Berridge at Jameson High School
(Click to enlarge)
I can still remember being fascinated by his lecture on the staircase phenomenon in the heart responding to adrenergic stimulation. I decided then that I would like to do a Ph.D. in insect physiology. At this stage the university in Rhodesia did not have a Ph.D. programme, but I was fortunate to obtain a Commonwealth Scholarship to do a Ph.D. in the Department of Zoology at the University of Cambridge with Sir Vincent Wigglesworth, the father of insect physiology.
My journey out of Africa was very exciting but also somewhat daunting as my new life in Cambridge was both different and challenging. Sir Vincent Wigglesworth arranged for me to be a member of Gonville and Caius College. For my PhD, I worked on nitrogen excretion of the African cotton stainer Dysdercus fasciatus, which enabled me to use my training in both chemistry and zoology. Towards the end of my thesis, I began to be interested in how fluid secretion by the Malpighian tubules was controlled and this is when my interest in cell signalling began. Some of the preliminary work I had done on the hormonal control of excretion formed the basis of a successful postdoctoral application to Professor Dietrich Bodenstein who was chairman of the Department of Biology at the University of Virginia in Charlottesville, which is a university town very similar to Cambridge.
Once I got my laboratory set up in America, my intention was to use blowfly Malpighian tubules as a model system to study hormone action. However, there was a problem in that the tubules failed to survive in vitro. I spent most of my time in Virginia unsuccessfully trying to develop a culture medium that would promote longer survival. I continued with this survival problem when I moved to Case Western Reserve University in Cleveland to work first in Michael Locke's laboratory in the Developmental Biology Center and then with Bodil Schmidt-Nielsen in the Dept of Biology. Despite much effort I made little progress and began to get increasingly desperate when my luck suddenly changed.
One day while dissecting out yet another Malpighian tubule to test out yet another culture medium, I noticed a long clear tube lying alongside the yellow-white Malpighian tubules. Out of curiosity, I dissected it out of the fly and set it up as for the Malpighian tubules and was astonished to find that this tiny tubule was secreting at rates 50 to 100 times those I had been recording with the Malpighian tubules. I soon found out that these tubes were the salivary glands that extend down the length of the fly. I also found out that the rapid secretion was controlled by the hormone 5-hydroxytryptamine (5-HT). In the absence of 5-HT, the glands were totally quiescent but upon addition of this agonist they began to secrete rapidly and the question arose as to how 5-HT was able to activate this secretory processes. As I began to read about this problem, I became aware of Sutherland and Rall's work on cyclic adenosine monophosphate (cyclic AMP) and their novel second messenger concept.
I was very excited about this idea that cyclic AMP acted as a second messenger to mediate the action of the first messenger that arrived at the cell surface such as the 5-HT in the case of my salivary glands. Imagine my excitement when I found that the stimulatory effect of 5-HT on fluid secretion was exactly duplicated by the addition of cyclic AMP. I was even more excited when I found out that Ted Rall, who had co-discovered cyclic AMP, was working in the Department of Pharmacology just across the road. I plucked up enough courage to go across to meet him and he turned out to be tremendously influential in helping me to understand the role of cyclic AMP in cell signalling. The old cliché of being in the right place at the right time was never more apt because I was helped enormously by frequent pharmacology tutorials from Ted Rall.
Ted Rall and Michael Berridge (Click to enlarge)
Through his help I was able to establish quickly that cyclic AMP was a key intracellular messenger in the insect salivary gland where it carried out the stimulatory action of 5-HT. My postdoctoral studies in America, which seemed to be heading for disaster, were ending on a high note as I began to search for a more permanent job. It was now time to leave my cosy postdoctoral existence to find a more permanent position. As I began to look for a job, a letter arrived from John Treherne in Cambridge offering me a position in a new Unit of Invertebrate Chemistry and Physiology he was setting up in the Zoology Department. The work I had done in Cleveland on cyclic AMP provided a robust working hypothesis to guide my new research programme. Having established that cyclic AMP was a messenger, the next obvious step was to find out how cyclic AMP carried out its role in stimulating fluid secretion. I approached this problem by characterizing the electrophysiological properties of the secretory response. I designed a small Perspex perfusion chamber that enabled me to monitor the trans-epithelial potential while adding and removing 5-HT or cyclic AMP. These experiments revealed that fluid secretion depended on the parallel flow of both potassium and chloride. It soon became clear that cyclic AMP controlled the flux of potassium, but something else was controlling the movement of chloride.
It soon became apparent that Ca2+ might regulate the passive flux of chloride. The most puzzling aspect of the Ca2+ messenger system in the insect blowfly was the source of Ca2+ much of which was derived from an internal store. Similar observations were also being made on various mammalian cells so the hunt was on to find the messenger that connected cell surface receptors to the internal store. The question was easy to define, but its solution seemed totally intractable. The aspect that frustrated me most was not having any idea of how to approach the problem. Finally, a way forward began to emerge from a somewhat unlikely direction when I became aware of the work by Hokin and Hokin on inositol lipids. In 1953, the Hokins discovered that an external agonist stimulated the turnover of a membrane lipid called phosphatidylinositol (PI) and this became known as the "PI response". However, its function remained somewhat mysterious for well over twenty years. This began to change in 1975 when Bob Michell suggested that lipid hydrolysis was responsible for Ca2+ signalling. I was intrigued by Michell's idea and began to search for the link between the PI response and Ca2+ signalling. In order to study the PI response, I had to descend into the murky world of biochemistry and developed a technique using radioactive inositol to measure the PI response in the salivary gland. In order to relate this hydrolysis of PI to Ca2+ signalling, it was necessary to have some way of measuring the latter. In a separate series of experiments, I devised a method of measuring Ca2+ signalling. Using these two techniques I was able to demonstrate that these two events were clearly related. However, there was no clue as to how the PI response at the cell membrane was able to liberate Ca2+ from the internal stores.
The photograph to the left (click to enlarge) was taken during a meeting at Lake Placid, USA in 1990. On the left is Bob Michell who was the first to suggest that the PI response may function in the control of Ca2+ signalling. Standing next to Michell is Lowell Hokin who together with his wife Mabel (sitting at the front) were the first to show that agonists stimulated the hydrolysis of phosphatidylinositol (PI). Standing next to the Hokins are Michael Berridge and Yasatomi Nishizuka who went on to show that this PI response functioned in Ca2+ signalling and the activation of protein phosphorylation by protein kinase C (PKC) respectively.
The discovery of the missing link began with some work on lithium. While taking time out to read the literature I came across some papers showing that lithium was a potent inhibitor of inositol phosphate metabolism and it was this work that directed me towards further biochemical studies. When I began to measure these inositiol phosphates, I was surprised to find that in addition to inositol monophosphate (IP1) that I was expecting, there were two additional peaks running after the IP1. On the basis of previous observations, these two peaks were likely to be inositol 1,4-bisphosphate (IP2) and inositol 1,4,5-trisphosphate (IP3). In order to confirm that these peaks were indeed IP2 and IP3, I needed to have some standards but these were not available from commercial sources. Once again, I was about to benefit from being in the right place.
As far as I could determine, there were only two sources at that time. One was in Clint Ballou's laboratory in Berkeley, California and the other was a few miles down the road in Rex Dawson's laboratory at the Babraham Institute. Rex Dawson and his colleague Robin Irvine were busily working on the identification of the enzymes that hydrolysed inositol lipids. Just as Ted Rall had proved invaluable in guiding me along the cyclic AMP path, Rex Dawson and Robin Irvine were very patient in helping me come to grips with the rather arcane world of inositol phosphate biochemistry. More importantly, tucked away in their freezer were a wide range of inositol phosphates and they kindly supplied me with the standards so that I could verify that the unknown peaks coming off my exchange columns were indeed IP2 and IP3.
In order to establish the kinetics of 5-HT-induced inositol phosphate formation, I developed a rapid perfusion system that enabled me to reveal that IP3 was being generated very quickly (within seconds) and it was this observation that led me to propose that IP3 might be the diffusible messenger that coupled the PI response to the mobilization of internal Ca2+. This was very much a eureka moment, because I can remember being very excited when I saw the results coming of the scintillation counter and felt that I had probably discovered something important. Indeed, my wife Susan still remembers my intense excitement when I arrived home to tell her about my discovery. Little did I know at the time just how significant this would turn out to be.
It is one thing to suggest how a second messenger might work but quite another to prove it. The experimental techniques to study the action of intracellular messengers are now relatively easy but twenty years ago it was very much more difficult. Not only was the supply of IP3 very limited, but also cellular injection techniques were poorly developed. While grappling with this problem, I attended a workshop in Amsterdam in December 1982 on "Biophysical and biochemical aspects of transcellular transport in animal tissues". The title of my lecture was "Phosphatidylinositol hydrolysis: a general transducing mechanism for calcium-mobilizing receptors". It was the first time that I had publicly put forward the idea that IP3 might be the long sought after Ca2+-mobilizing second messenger.
In the same session, Irene Schulz described a permeabilized pancreatic cell preparation where she was able to gain access to the internal Ca2+ stores. This was exactly what I was looking for to test out the proposed function of IP3 and she was more than happy to set up a collaborative study. On returning to Cambridge, I contacted Robin Irvine who agreed to prepare the large amounts of IP3 that were required for these permeabilized cell experiments. A few weeks after I had sent the samples to Germany, I received an excited phone call to say that IP3 had mobilized Ca2+ and the paper summarizing our results was published in Nature towards the end of 1983.
Once our paper appeared in Nature, we were contacted by a number of groups anxious to try out this new messenger on their cells. We set up a number of collaborations and within a very short period we were able to confirm that IP3 released Ca2+ in many different cell types and it soon became clear that IP3 was indeed the Ca2+-mobilizing second messenger we had all been looking for. It had taken 30 years since the discovery of the PI response by Hokin and Hokin in 1953 to finally find out that one of its functions is to generate a second messenger to stimulate the release of internal Ca2+.
Michael Berridge, Irene Schulz and Robin Irvine
(Click to enlarge)
The discovery that IP3 was a universal second messenger controlling Ca2+ signalling completely changed my life and it heralded a new phase in my research career. Having spent so much time doing biochemistry, I was anxious to return to physiology, which I did by turning my attention to the spatial and temporal aspects of Ca2+ signalling. One of the questions I am asked most frequently is how can this messenger regulate so many different processes, in some instances within the same cell. We soon learnt that much of this remarkable versatility depends on the way information is encoded in the spatial and temporal organization of Ca2+ signals. My interest in these spatiotemporal aspects began with studies on Ca2+ oscillations and I then turned to the spatial aspects using single cell imaging techniques.
In 1986 I visited Roger Tsien at Berkeley and was shown his new purpose built imaging system and immediately realized the significance of this new technology. I obtained the funds to set up such a system in Cambridge. For some one who had been studying covert Ca2+ signalling for so long, it was an awe-inspiring experience to visualize how Ca2+ signals are generated in cells. The spiral waves that pulsate through the cytoplasm of Xenopus oocytes are objects of great beauty. Using this new technology has enabled us and other groups to unveil just how important the spatial organization of the InsP3/Ca2+ signalling system is in regulating cellular activity. Some of the most exciting work to emerge from Martin Bootman's laboratory at Babraham has shown that the release of Ca2+ by InsP3 has an important function in the heart and is providing new insights into the pathology of cardiac arrhythmias.
My life in Cambridge has been enriched by my fellowship at Trinity College. During my career I have received a number of honours and awards. I was elected a Fellow of The Royal Society in 1984. In 1999 I was elected to both the National Academy of Sciences and the American Academy of Arts and Sciences. In 2007 I became a member of the American Philosophical Society.
One of my proudest moments was to go to Buckingham Palace to be knighted by the Queen for 'service to science' (click to enlarge photograph on right).
My work on second messengers has also been acknowledged by a number of prizes such as The King Faisal International Prize in Science, The Louis Jeantet Prize in Medicine, The Albert Lasker Medical Research Award, The Heineken Prize for Biochemistry and Biophysics, The Wolf Foundation Prize in Medicine and, most recently, The Shaw Prize in Life Science and Medicine (2005).
Further information is available in:
Berridge, M.J. (2005) Unlocking the secrets of cell signalling. Annu.Rev.Physiol. 67: 1-21.
Gatooma, Rhodesia, 22 October 1938
1960 BSc University College of Rhodesia and Nyasaland,
Salisbury, Rhodesia, 1st Class honours
1965 PhD University of Cambridge (Supervisor: Sir Vincent B Wigglesworth)
1965-66 Post-doctoral Fellow, University of Virginia (Prof. D.Bodenstein)
1966-67 Post-doctoral Fellow, Case Western Reserve University (with Dr M Locke)
1967-69 Research Associate, Case Western University (with Dr B Schmidt-Nielsen)
1969-72 Senior Scientific Officer, Unit of Invertebrate Chemistryand Physiology (Director Dr JE Treherne), University of Cambridge
1972-78 Principal Scientific Officer, Unit of Invertebrate Chemistry and Physiology, Cambridge
1978-90 Senior Principal Scientific Officer, Unit of Insect Neurophysiology and Pharmacology, Cambridge
1990-96 Deputy Chief Scientific Officer (Grade 4), Laboratory of Molecular Signalling, Babraham Institute
1996-2003 Head of Signalling, Babraham Institute
1972-86 Elected Title C Fellow, Trinity College, Cambridge
1986 Elected Title B Fellow, Trinity College, Cambridge
1984 Elected Fellow of The Royal Society
1994- Honorary Professor of Cell Signalling (University of Cambridge)
1998 Honorary Fellowship- Gonville and Caius College, Cambridge
2003- Emeritus Babraham Fellow
Honorary Member of the Japanese Biochemical Society
Society of General Physiologists
1989 Academia Europaea
1991 European Molecular Biology Organization (EMBO)
1992 Honorary Member of the American Physiological Society
1994 Foreign Correspondent of The Academie Royale de Medecine de Belgique
1995 Honorary Life Member of The Society for Experimental Biology
1998 The Academy of Medical Sciences (London)
1999 National Academy of Science (Foreign Associate) (Washington, DC)
1999 American Academy of Arts and Science (Foreign Honorary Member)
2000 Honorary Fellowship of the Institute of Biology
2004 Honorary Member of the Biochemical Society
2006 Honorary Member of the European Calcium Society
2007 American Philosophical Society
1984 Annual Bayer AG Lecture in Pharmacology (Yale University School of Medicine)
1985 Halliburton Lecture (Kings College, London)
1985 Harrison Lecture (Endocrine Society of Australia)
1986 Nelson Medical Lecture (University of California, Davis)
1987 Wellcome Visiting Professor (Medical School, The University of Texas)
1987 The N I H Lecture
1987 ICI Prize Lecture (University of Manchester)
1987 The Baule Distinguished Lecture in Neuroscience (Syracuse)
1987 The Alice and Joseph Brooks International Lecture in Neurosciences (Harvard Medical School)
1988 16th FEBS Ferdinand Springer Lecturer
1988 Royal Society Croonian Lecture
1988 18th Annual Schueler Distinguished Lecture in Pharmacology (Tulane University)
1988 Smith Kline and French Lecture (University of London)
1988 2nd Hillarp Lecture (European Neurosciences Association (Zurich)
1988 Ralph Dorfman Lecture (Stanford University School of Medicine)
1988 Steinhouse Memorial Lecture (University of California, Irvine)
1988 Robert E. Olsen Lecture (St.Louis University School of Medicine)
1988 Hillarp Memorial Lecture (Bioscience 88, Malmo, Sweden)
1989 Harold Lamport Lecture (University of Washington, Seattle)
1989 Flexner Lecture (Vanderbilt University, Nashville)
1989 Chilton Lecture (University of Texas, Dallas)
1989 Boxer Lecture (University of Medicine and Dentistry of New Jersey)
1989 Samuel Rudin Visiting Professorship (Columbia University)
1990 Dame Honor B. Fell Lecture (Cardiff)
1990 Charnock Bradley Memorial Lecture (University of Edinburgh)
1990 John R. Murlin Lecture (University of Rochester)
1990 College of Medicine Distinguished Lecturer (University of lowa)
1990 Leslie L. Bennett Lecture (University of California, S.F.)
1990 The Inaugural Albert L. Lehninger Lecture (The Johns Hopkins University, Baltimore)
1991 Frank Rose Memorial Lecture (British Association for Cancer Research)
1991 Falk Memorial Lecture (NIEHS, Research Triangle Park)
1991 The ICI Guest Lecture (Medical Research Society, UK)
1992 The 19th Annual Calbiochem Lectureship in Chemistry (University of California, San Diego)
1992 The Poulsson Lecture (University of Oslo)
1993 The Donald W Seldin Lecture (The 12th International Congress of Nephrology, Jerusalem)
1994 The 14th Dr Abraham White Memorial Lecture (Syntex, Palo Alto, California)
1994 Storer Life Sciences Lecture (University of California, Davis)
1995 Bidder Lecture (The Society for Experimental Biology)
1995 Hugh Davson Distinguished Lectureship (The American Physiological Society)
1996 Applebaum Distinguished Lecturer (The University of Florida, Gainesville)
1996 Annual Review Prize Lecture (The Physiological Society)
1996 Dr Aaron I. Grollman Visiting Lectureship in Basic Medical Sciences (University of Maryland, Baltimore)
1997 6th Choh Hao Li Memorial Lecturer (Berkeley, California)
2001 Edwin G. Krebs Lecture in Molecular Pharmacology (University of Washington School of Medicine, Seattle.
1999 First Fred Fay Lecture (Dept. of Physiology, Univ. of Massachusetts Medical School).
2000 Alvin Taurog Lecture (The University of Texas, Southwestern Medical Center, Dallas)
2000 Lister Memorial Lecture (Society of Chemical Industry, Edinburgh)
2002 The Dean's Lecture (Mt. Sinai School of Medicine (New York)
2004 23rd Steinberg/Wylie Lecture (Univ, of Maryland School of Medicine)
2004 The Seventh Annual Nathan S. Greenfield Family Lecture (Dept. of Pharmacology, Case Western Reserve University School of Medicine
2004 Paul D. Lamson Lecture (Dept. of Pharmacology, Vanderbilt University Medical Center
2006 The Raymond and Beverly Sackler Distinguished Lecture (Dept. of Medicine, University of Cambridge)
2006 The Leopold Koss Lecture (University of Bern)
2007 The Gerald D Aurbach Memorial Lecture (The American Society for Bone and Mineral Research)
1998 Knight Bachelor
1993 Degree of Doctor Honoris Causa (Limburgs Universitair Centrum, Belgium)
2007 Honorary Degree, University of Liverpool
1989 Baly Medal (Royal College of Physicians, London)
1990 Dale Medal (Society for Endocrinology)
1991 Royal Medal (The Royal Society)
1984 Feldberg Prize
1986 The King Faisal International Prize in Science
1986 Louis Jeantet Prize in Medicine
1987 William Bate Hardy Prize (Cambridge Philosophical Society)
1987 Abraham White Scientific Achievement Award (George Washington University School of Medicine)
1988 Gairdner Foundation International Award
1989 Albert Lasker Basic Medical Research Award
1990 Rita Levi Montalcini Award Lecture (Fidia Research Foundation, Washington DC)
1991 CIBA-GEIGY/DREW Award in Biomedical Research
1994 Dr H P Heineken Prize for Biochemistry and Biophysics
1995 The Wolf Foundation Prize in Medicine (Israel)
1996 The Massry Prize in Nephrology, Physiology and Related Fields (Meira and Shaul G. Massry Foundation, USA)
1999 Ernst Schering Prize (Ernst Schering Research Foundation, Berlin)
2005 The Shaw Prize in Life Science and Medicine (Press release)
Fain, J.N. & Berridge, M.J. (1979) Relationship between hormonal activation of phosphatidylinositol hydrolysis, fluid secretion and calcium flux in the blowfly salivary gland.
Biochem. J. 178: 45-48
Fain, J.N. & Berridge, M.J. (1979) Relationship between phosphatidylinositol synthesis and recovery of 5-hydroxytryptamine responsive-Ca2+ flux in blowfly salivary gland.
Biochem. J. 180: 655-661.
Berridge, M.J., Downes, C.P. & Hanley, M.R. (1982) Lithium amplifies agonist-dependent phosphatidylinositol responses in brain and salivary glands.
Biochem. J. 206: 587-595.
Berridge, M.J., Dawson, R.M.C., Downes, C.P., Heslop, J.P. & Irvine, R.F. (1983) Changes in the levels of inositol phosphates after agonist- dependent hydrolysis of membrane phosphoinositides.
Biochem. J. 212: 473-482.
Berridge, M.J. (1983) Rapid accumulation of inositol trisphosphate reveals that agonists hydrolyse polyphosphoinositides instead of phosphatidylinositol.
Biochem. J. 212: 849-858.
Streb, H., Irvine, R.F., Berridge, M.J. & Schulz, I. (1983) Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol 1,4,5-trisphosphate.
Nature (Lond.) 306: 67-69.
Irvine, R.F., Letcher, A.J., Heslop, J.P. & Berridge, M.J. (1986) The inositol tris/tetrakisphosphate pathway - demonstration of Ins 1,4,5P3 3-kinase activity in animal cells.
Nature (Lond.) 320: 631-634.
Rapp, P.E. & Berridge, M.J. (1981) The control of transepithelial potential oscillations in the salivary gland of Calliphora erythrocephala.
J. Exp. Biol. 93: 119-132.
Missiaen, L., Taylor, C.W. & Berridge, M.J. (1991) Spontaneous calcium release from inositol trisphosphate-sensitive calcium stores.
Nature 352: 241-244.
Petersen, C.C. H. & Berridge, M.J. (1994) The regulation of capacitative calcium entry by calcium and PKC in Xenopus oocytes.
J. Biol. Chem. 269, 32246-32253.
McGuinness, O.M., Moreton, R.B., Johnson, M.H. & Berridge, M.J. (1996) A direct measurement of increased divalent cation influx in fertilized mouse oocytes.
Development 122, 2199-2206.
Bootman, M.D., Berridge, M.J. & Lipp, P. (1997) Cooking with calcium: The recipes for composing global signals from elementary events
Cell 91, 367-373.
Koizumi, S., Bootman, M.D., Bobanović, L.K. Schell, M.J., Berridge, M.J. & Lipp, P. (1999) Characterization of elementary Ca2+ release signals in NGF-differentiated PC12 cells and hippocampal neurons.
Neuron 22: 125-137.
Mackenzie, L., Bootman, M.D., Berridge, M.J. & Lipp, P. (2001) Predetermined recruitment of calcium release sites underlies excitation-contraction coupling in rat atrial myocytes.
J. Physiol. 530:417-429.
Collins, T.J., Berridge, M.J., Lipp, P. & Bootman, M.D. (2002) Mitochondria are morphologically and functionally heterogeneous within cells.
EMBO J. 21:1616-1627.
Chen, R., Valencia, I., Zhong, F., McColl, K.S. Roderick, H.L., Bootman, M.D., Berridge, M.J., Conway, S.J., Holmes, A.B., Mignery, G.A., Velez, P. & Distelhorst, C.W. (2004) Bcl-2 functionally interatcs with inositol 1,4,5-trisphosphate receptors to regulate calcium release from the ER in response to inositol 1,4,5-trisphosphate.
J.Cell Biol. 166: 193-203.
Mackenzie,L., Roderick, H.L., Berridge, M.J., Conway, S.J. & Bootman, M.D.(2004) The spatial pattern of atrial cardiomyocyte calcium signalling modulates contraction.
J Cell Sci. 117: 6327-6337.
Proven, A., Roderick, H.L., Conway, S.J., Berridge, M.J., Horton, J.K. Capper, S.J. and Bootman, M.D. (2006) Inositol 1,4,5-trisphosphate supports the arrhythmogenic action of endothelin-1 on ventricular cardiac myocytes.
J. Cell Sci. 119: 3363-3375.
Berridge, M.J. & Irvine, R.F. (1984) Inositol trisphosphate, a novel second messenger in cellular signal transduction.
Nature 312: 315-321.
Berridge, M.J. (1987) Inositol trisphosphate and diacylglycerol: two interacting second messengers.
Ann. Rev. Biochem. 56: 159-193.
Berridge, M.J. & Irvine, R.F. (1989) Inositol phosphates and cell signalling.
Nature (Lond.) 341: 197-205.
Berridge, M.J., Downes, C.P. & Hanley, M.R. (1989) Neural and developmental actions of lithium: A unifying hypothesis.
Cell 59: 411-419.
Berridge, M.J. (1993) Inositol trisphosphate and calcium signalling.
Nature 361: 315-325.
Bootman, M.D. & Berridge, M.J. (1995) The elemental principles of calcium signalling.
Cell 83: 675-678.
Berridge, M.J. (1995) Capacitative calcium entry.
Biochem. J. 312, 1-11.
Berridge, M.J. (1998) Neural calcium signalling.
Neuron 21, 13-26.
Berridge, M.J., Lipp, P. & Bootman, M.D. (2000) The versatility and universality of calcium signalling.
Nature Rev. Mol.Cell Biol. 1: 11-21.
Berridge, M.J. (2003) The endoplasmic reticulum: a multifunctional signaling organelle.
Cell Calcium. 32: 235-249.
Berridge, M.J., Bootman, M.D. & Roderick, H.L. (2003) Calcium signalling: Dynamics, homeostasis and remodelling.
Nature Rev. Mol.Cell Biol. 4:517-529.
Berridge, M.J. (2004) Conformational coupling: A physiological calcium entry mechanism.
Sci. STKE 2004,pe33.
Berridge, M.J. (2006) Calcium microdomains: Organization and function.
Cell Calcium 40: 405-412.
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