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4. Contributors

Author

Arumugasamy, Shiva Kumar, primary, Atmakuru, Ramesh, additional, Balaji, Meriga, additional, Basha, Pinjari Aleem, additional, Begum, Pathan Shajahan, additional, Chakravarthy, Harshini, additional, Chandra, M. Neethi, additional, Chandra, Muni Ramanna Gari Subhosh, additional, Charyulu, P. B. B.N., additional, Chellasamy, Gayathri, additional, Chippada, Appa Rao, additional, Chunduri, Venkata Rao, additional, Devanathan, Vasudharani, additional, Devi, Mekala Charitha, additional, Galla, Krishna Murthy Naidu, additional, Gopi Krishna, Pitchika, additional, Govindaraju, Saravanan, additional, Gowthami, K., additional, Gunavathi, Y., additional, Gundi, Vijay A.K.B., additional, Gurushankara, Hunasanahally Puttaswamygowda, additional, Hanuma Kumar, Ghali E.N., additional, Heleena Hemavathy, C.V., additional, Hema, M., additional, Jaya Madhuri, R., additional, Jyothi Reddy, G., additional, Kalyanasundaram, Geetha Thanuja, additional, Kameswaran, S., additional, Karri, Satyanagalakshmi, additional, Kathera, Chandrasekhar, additional, Kumar Katikala, Ravi, additional, Kim, Jongsung, additional, Kim, Sanghyo, additional, Koduru, Swetha Kumari, additional, Konakalla, Naga Charan, additional, Lakshmi, Buddolla Anantha, additional, Marella, Saritha, additional, Maurya, Dharmendra K., additional, Naidu, Lankipalli Tharachand, additional, Naveen, Thanjavur, additional, Naveen Taj, S., additional, Nimgampalle, Mallikarjuna, additional, Nirmal Kumar, A.R., additional, Nithya, S., additional, Niveditha, B.T., additional, Palempalli, Uma Maheswari Devi, additional, Paul, Pandeeti Emmanuel Vijay, additional, Pooja, M., additional, Raffi, Mokula Mohammed, additional, Rajagopal, Senthilkumar, additional, Rajakumari, Devarapogu, additional, Rajasrerlatha, V., additional, Raju, C., additional, Ramesh, Rayi, additional, Rani, Asupatri Usha, additional, Razak, Meerza Abdul, additional, Reddy, Ankireddy Seshadri, additional, Rupak, Kumar, additional, Sangubotla, Roopkumar, additional, Shubha, D., additional, Singh, Manpreet, additional, Sistla, Durga Srinivasa Murthy, additional, Sri Ranjani, T., additional, Srinivas, Kalanghad P., additional, Subburamu, Karthikeyan, additional, Suman, Kapur, additional, Syed, Nyamath, additional, Tadepally, Hamsa D., additional, Thippeswamy, M., additional, Thirumalanadhuni, Vasavi, additional, Tollamadugu, N.V.K.V. Prasad, additional, Tyagi, Vikrant, additional, Vadela, Manohar Babu, additional, Viswanath, Buddolla, additional, Vulichi, Srinivasa Rao, additional, Yadav, Panyam Suresh, additional, Yasaswini, G., additional, Yerraguravagari, Lavanya Latha, additional, and Yun, Kyusik, additional

Published
2021
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7. List of contributors

Author

Anjana, Bosetty, primary, Ankireddy, Seshadri Reddy, additional, Banavath, Hemanth Naick, additional, Belagal, Praveen, additional, Belliraj, Siva Kumar, additional, Bonilla-Aldana, D. Katterine, additional, Chellasamy, Gayathri, additional, Dakshinamurthy, Soumya, additional, Dasari, Subramanyam, additional, Devanathan, Vasudharani, additional, Dhingra, Niyati, additional, Gonsalves, Rhea Conchita, additional, Gopal, Divi Venkata Ramana Sai, additional, Govindaraju, Saravanan, additional, Gurushankara, Hunasanahally Puttaswamygowda, additional, Hense, Sibasis, additional, Karyala, Prashanthi, additional, Kim, Jongsung, additional, Kiriyanthan, Rose Mary, additional, Kishore, Kamal, additional, Konakalla, Naga Charan, additional, Kusuma, Kandati, additional, Mallikarjunaiah, Shanthala, additional, Manohar, Sai, additional, Masarapu, Hema, additional, Metikurki, Basavaraja, additional, Mukherjee, Pratik, additional, Nimgampalle, Mallikarjuna, additional, Pacharla, Himavani, additional, Pakala, Suresh B., additional, Paul, Pandeeti Emmanuel Vijay, additional, Radha, A., additional, Rathod, Kajal, additional, Rodriguez-Morales, Alfonso J., additional, Sangubotla, Roopkumar, additional, Saxena, Ambrish, additional, Singh, Manpreet, additional, Singh, Neha, additional, Srinivas, Kalanghad P., additional, Thippeswamy, Nayaka Boramuthi, additional, Tripathi, Ekta, additional, Viswanath, Buddolla, additional, and Yun, Kyusik, additional

Published
2021
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15. Selective protection of murine cerebral Gi/o-proteins from inactivation by parenterally injected pertussis toxin

Author

Vega, Salvador Castaneda, primary, Leiss, Veronika, additional, Piekorz, Roland, additional, Calaminus, Carsten, additional, Pexa, Katja, additional, Vuozzo, Marta, additional, Schmid, Andreas M., additional, Devanathan, Vasudharani, additional, Kesenheimer, Christian, additional, Pichler, Bernd J., additional, Beer-Hammer, Sandra, additional, and Nürnberg, Bernd, additional

Published
2019
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20. Adaptive gene regulation in the striatum of RGS9-deficient mice

Author

Busse, Kathy, Strotmann, Rainer, Strecker, Karl, Wegner, Florian, Devanathan, Vasudharani, Gohla, Antje, Schöneberg, Torsten, Schwarz, Johannes, Universität Leipzig, Universität Tübingen, Universität Würzburg, and Technische Universität München

Subjects
Male, Cell signaling, Dyskinesia, Drug-Induced, Gene Expression, lcsh:Medicine, Signal transduction, ERK signaling cascade, Mice, Molecular Cell Biology, Medicine and Health Sciences, Cyclic AMP, Phosphorylation, lcsh:Science, Movement Disorders, Neuronal Plasticity, G-Protein, Signal, Proteinkinase, Maus, Signaling cascades, Neurodegenerative Diseases, Parkinson Disease, Animal Models, cAMP signaling cascade, Neurology, Calcium signaling cascade, Research Article, Cell biology, MAPK signaling cascades, Adenylyl Cyclase Signaling Pathway, Mouse Models, Research and Analysis Methods, Model Organisms, Calcium-Mediated Signal Transduction, Genetics, Animals, Calcium Signaling, ddc:610, Adenylyl cyclase signaling cascade, Biology and life sciences, Receptors, Dopamine D2, Long-Term Synaptic Depression, lcsh:R, Neostriatum, G-Protein Signaling, Gene Expression Regulation, Cellular Neuroscience, Synapses, G-protein signaling, Protein kinase signaling, mouse, lcsh:Q, sense organs, Molecular Neuroscience, RGS Proteins, Neuroscience
Abstract

Background: RGS9-deficient mice show drug-induced dyskinesia but normal locomotor activity under unchallenged conditions. Results: Genes related to Ca2+ signaling and their functions were regulated in RGS9-deficient mice. Conclusion: Changes in Ca2+ signaling that compensate for RGS9 loss-of-function can explain the normal locomotor activity in RGS9-deficient mice under unchallenged conditions. Significance: Identified signaling components may represent novel targets in antidyskinetic therapy. The long splice variant of the regulator of G-protein signaling 9 (RGS9-2) is enriched in striatal medium spiny neurons and dampens dopamine D2 receptor signaling. Lack of RGS9-2 can promote while its overexpression prevents drug-induced dyskinesia. Other animal models of drug-induced dyskinesia rather pointed towards overactivity of dopamine receptor-mediated signaling. To evaluate changes in signaling pathways mRNA expression levels were determined and compared in wild-type and RGS9- deficient mice. Unexpectedly, expression levels of dopamine receptors were unchanged in RGS9-deficient mice, while several genes related to Ca2+ signaling and long-term depression were differentially expressed when compared to wild type animals. Detailed investigations at the protein level revealed hyperphosphorylation of DARPP32 at Thr34 and of ERK1/2 in striata of RGS9-deficient mice. Whole cell patch clamp recordings showed that spontaneous synaptic events are increased (frequency and size) in RGS9-deficient mice while long-term depression is reduced in acute brain slices. These changes are compatible with a Ca2+-induced potentiation of dopamine receptor signaling which may contribute to the drug-induced dyskinesia in RGS9-deficient mice.:Introduction; Materials and methods; Results; Discussion

Published
2014

21. The plexin C1 receptor promotes acute inflammation

Author

König, Klemens, primary, Marth, Linda, additional, Roissant, Jan, additional, Granja, Tiago, additional, Jennewein, Carla, additional, Devanathan, Vasudharani, additional, Schneider, Mariella, additional, Köhler, David, additional, Zarbock, Alexander, additional, and Rosenberger, Peter, additional

Published
2014
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22. Gαi2- and Gαi3-Deficient Mice Display Opposite Severity of Myocardial Ischemia Reperfusion Injury

Author

Köhler, David, primary, Devanathan, Vasudharani, additional, Bernardo de Oliveira Franz, Claudia, additional, Eldh, Therese, additional, Novakovic, Ana, additional, Roth, Judith M., additional, Granja, Tiago, additional, Birnbaumer, Lutz, additional, Rosenberger, Peter, additional, Beer-Hammer, Sandra, additional, and Nürnberg, Bernd, additional

Published
2014
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24. Downregulation of the renal outer medullary K+ channel ROMK by the AMP-activated protein kinase

Author

Siraskar, Balasaheb, primary, Huang, Dan Yang, additional, Pakladok, Tatsiana, additional, Siraskar, Gulab, additional, Sopjani, Mentor, additional, Alesutan, Ioana, additional, Kucherenko, Yulia, additional, Almilaji, Ahmad, additional, Devanathan, Vasudharani, additional, Shumilina, Ekaterina, additional, Föller, Michael, additional, Munoz, Carlos, additional, and Lang, Florian, additional

Published
2012
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25. Gαi2- and Gαi3-Deficient Mice Display Opposite Severity of Myocardial Ischemia Reperfusion Injury.

Author

Köhler, David, Devanathan, Vasudharani, Bernardo de Oliveira Franz, Claudia, Eldh, Therese, Novakovic, Ana, Roth, Judith M., Granja, Tiago, Birnbaumer, Lutz, Rosenberger, Peter, Beer-Hammer, Sandra, and Nürnberg, Bernd

Subjects
*G protein coupled receptors, *CORONARY disease, *REPERFUSION injury, *LABORATORY mice, *IMMUNOFLUORESCENCE, *CELLULAR signal transduction, *MYOCARDIAL infarction
Abstract

G-protein-coupled receptors (GPCRs) are the most abundant receptors in the heart and therefore are common targets for cardiovascular therapeutics. The activated GPCRs transduce their signals via heterotrimeric G-proteins. The four major families of G-proteins identified so far are specified through their α-subunit: Gαi, Gαs, Gαq and G12/13. Gαi-proteins have been reported to protect hearts from ischemia reperfusion injury. However, determining the individual impact of Gαi2 or Gαi3 on myocardial ischemia injury has not been clarified yet. Here, we first investigated expression of Gαi2 and Gαi3 on transcriptional level by quantitative PCR and on protein level by immunoblot analysis as well as by immunofluorescence in cardiac tissues of wild-type, Gαi2-, and Gαi3-deficient mice. Gαi2 was expressed at higher levels than Gαi3 in murine hearts, and irrespective of the isoform being knocked out we observed an up regulation of the remaining Gαi-protein. Myocardial ischemia promptly regulated cardiac mRNA and with a slight delay protein levels of both Gαi2 and Gαi3, indicating important roles for both Gαi isoforms. Furthermore, ischemia reperfusion injury in Gαi2- and Gαi3-deficient mice exhibited opposite outcomes. Whereas the absence of Gαi2 significantly increased the infarct size in the heart, the absence of Gαi3 or the concomitant upregulation of Gαi2 dramatically reduced cardiac infarction. In conclusion, we demonstrate for the first time that the genetic ablation of Gαi proteins has protective or deleterious effects on cardiac ischemia reperfusion injury depending on the isoform being absent. [ABSTRACT FROM AUTHOR]

Published
2014
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26. Cellular Form of Prion Protein Inhibits Reelin-Mediated Shedding of Caspr from the Neuronal Cell Surface to Potentiate Caspr-Mediated Inhibition of Neurite Outgrowth.

Author

Devanathan, Vasudharani, Jakovcevski, Igor, Santuccione, Antonella, Shen Li, Hyun Joon Lee, Peles, Elior, Leshchyns'ka, Iryna, Sytnyk, Vladimir, and Schachner, Melitta

Subjects
*AXONS, *DENDRITES, *CELL membranes, *CENTRAL nervous system, *SPINAL cord injuries
Abstract

Extension of axonal and dendritic processes in the CNS is tightly regulated by outgrowth-promoting and -inhibitory cues to assure precision of synaptic connections. We identify a novel role for contactin-associated protein (Caspr) as an inhibitory cue that reduces neurite outgrowth from CNS neurons. We show that proteolysis of Caspr at the cell surface is regulated by the cellular form of prion protein (PrP), which directly binds to Caspr. PrP inhibits Reelin-mediated shedding of Caspr from the cell surface, thereby increasing surface levels of Caspr and potentiating the inhibitory effect of Caspr on neurite outgrowth. PrP deficiency results in reduced levels of Caspr at the cell surface, enhanced neurite outgrowth in vitro, and more efficient regeneration of axons in vivo following spinal cord injury. Thus, we reveal a previously unrecognized role for Caspr and PrP in inhibitory modulation of neurite outgrowth in CNS neurons, which is counterbalanced by the proteolytic activity of Reelin. [ABSTRACT FROM AUTHOR]

Published
2010
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27. Platelet Gi protein Gαi2 is an essential mediator of thrombo-inflammatory organ damage in mice.

Author

Devanathan V, Hagedorn I, Köhler D, Pexa K, Cherpokova D, Kraft P, Singh M, Rosenberger P, Stoll G, Birnbaumer L, Piekorz RP, Beer-Hammer S, Nieswandt B, and Nürnberg B

Subjects
Animals, Bleeding Time, Blood Platelets metabolism, GTP-Binding Protein alpha Subunit, Gi2 deficiency, Immunoblotting, Megakaryocytes metabolism, Mice, Reperfusion Injury prevention & control, GTP-Binding Protein alpha Subunit, Gi2 metabolism, Infarction, Middle Cerebral Artery physiopathology, Inflammation physiopathology, Platelet Activation physiology, Reperfusion Injury physiopathology, Thrombosis physiopathology
Abstract

Platelets are crucial for hemostasis and thrombosis and exacerbate tissue injury following ischemia and reperfusion. Important regulators of platelet function are G proteins controlled by seven transmembrane receptors. The Gi protein Gα(i2) mediates platelet activation in vitro, but its in vivo role in hemostasis, arterial thrombosis, and postischemic infarct progression remains to be determined. Here we show that mice lacking Gα(i2) exhibit prolonged tail-bleeding times and markedly impaired thrombus formation and stability in different models of arterial thrombosis. We thus generated mice selectively lacking Gα(i2) in megakaryocytes and platelets (Gna(i2)(fl/fl)/PF4-Cre mice) and found bleeding defects comparable to those in global Gα(i2)-deficient mice. To examine the impact of platelet Gα(i2) in postischemic thrombo-inflammatory infarct progression, Gna(i2)(fl/fl)/PF4-Cre mice were subjected to experimental models of cerebral and myocardial ischemia/reperfusion injury. In the model of transient middle cerebral artery occlusion stroke Gna(i2)(fl/fl)/PF4-Cre mice developed significantly smaller brain infarcts and fewer neurological deficits than littermate controls. Following myocardial ischemia, Gna(i2)(fl/fl)/PF4-Cre mice showed dramatically reduced reperfusion injury which correlated with diminished formation of the ADP-dependent platelet neutrophil complex. In conclusion, our data provide definitive evidence that platelet Gα(i2) not only controls hemostatic and thrombotic responses but also is critical for the development of ischemia/reperfusion injury in vivo.

Published
2015
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