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145 results on '"Ghose, Aurnab"'

1. Immunogenicity of SARS-CoV-2 vaccines BBV152 (COVAXIN®) and ChAdOx1 nCoV-19 (COVISHIELD™) in seronegative and seropositive individuals in India: a multicentre, nonrandomised observational study

Author

Asokan, Mangaiarkarasi S., Joan, Roshni Florina, Babji, Sudhir, Dayma, Girish, Nadukkandy, Prajitha, Subrahmanyam, Vinutha, Pandey, Archana, Malagi, Girish, Arya, Pooja, Mahajan, Vibhuti, Bhavikatti, Jayateerth, Pawar, Ketakee, Thorat, Aishwarya, Shah, Priyanki, Goud, Ramakrishna B., Roy, Bishnudeo, Rajukutty, Shon, Immanuel, Sushil, Agarwal, Dhiraj, Saha, Sankhanil, Shivaraj, Akshatha, Panikulam, Patricia, Shome, Rajeshwari, Gulzar, Shah-E-Jahan, Sharma, Anusmrithi U., Naik, Ajinkya, Talashi, Shruti, Belekar, Madhuri, Yadav, Ritu, Khude, Poornima, V, Mamatha, Shivalingaiah, Sudarshan, Deshmukh, Urmila, Bhise, Chinmayee, Joshi, Manjiri, Inbaraj, Leeberk Raja, Chandrasingh, Sindhulina, Ghose, Aurnab, Jamora, Colin, Karumbati, Anandi S., Sundaramurthy, Varadharajan, Johnson, Avita, Ramesh, Naveen, Chetan, Nirutha, Parthiban, Chaitra, Ahmed, Asma, Rakshit, Srabanti, Adiga, Vasista, D'souza, George, Rale, Vinay, George, Carolin Elizabeth, John, Jacob, Kawade, Anand, Chaturvedi, Akanksha, Raghunathan, Anu, Dias, Mary, Bhosale, Anand, Raghu, Padinjat, Shashidhara, L.S., Vyakarnam, Annapurna, Bal, Vineeta, Kang, Gagandeep, and Mayor, Satyajit

Published
2024
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2. A tale of two waves: Delineating diverse genomic and transmission landscapes driving the COVID-19 pandemic in Pune, India

Author

Niveditha, Divya, Khan, Soumen, Khilari, Ajinkya, Nadkarni, Sanica, Bhalerao, Unnati, Kadam, Pradnya, Yadav, Ritu, Kanekar, Jugal B., Shah, Nikita, Likhitkar, Bhagyashree, Sawant, Rutuja, Thakur, Shikha, Tupekar, Manisha, Nagar, Dhriti, Rao, Anjani G., Jagtap, Rutuja, Jogi, Shraddha, Belekar, Madhuri, Pathak, Maitreyee, Shah, Priyanki, Ranade, Shatakshi, Phadke, Nikhil, Das, Rashmita, Joshi, Suvarna, Karyakarte, Rajesh, Ghose, Aurnab, Kadoo, Narendra, Shashidhara, LS, Monteiro, Joy Merwin, Shanmugam, Dhanasekaran, Raghunathan, Anu, and Karmodiya, Krishanpal

Published
2023
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5. Antagonistic Activities of Fmn2 and ADF Regulate Axonal F-Actin Patch Dynamics and the Initiation of Collateral Branching

Author

Kundu, Tanushree, Siva Das, Sooraj, Sewatkar, Lisas K., Kumar, Divya S., Nagar, Dhriti, and Ghose, Aurnab

Subjects
Actin Cytoskeleton, General Neuroscience, Animals, Research Articles, Actins, Zebrafish
Abstract

Interstitial collateral branching of axons is a critical component in the development of functional neural circuits. Axon collateral branches are established through a series of cellular processes initiated by the development of a specialized, focal F-actin network in axons. The formation, maintenance and remodeling of this F-actin patch is critical for the initiation of axonal protrusions that are subsequently consolidated to form a collateral branch. However, the mechanisms regulating F-actin patch dynamics are poorly understood. Fmn2 is a formin family member implicated in multiple neurodevelopmental disorders. We find that Fmn2 regulates the initiation of axon collateral protrusions in chick spinal neurons and in zebrafish motor neurons. Fmn2 localizes to the protrusion-initiating axonal F-actin patches and regulates the lifetime and size of these F-actin networks. The F-actin nucleation activity of Fmn2 is necessary for F-actin patch stability but not for initiating patch formation. We show that Fmn2 insulates the F-actin patches from disassembly by the actin-depolymerizing factor, ADF, and promotes long-lived, larger patches that are competent to initiate axonal protrusions. The regulation of axonal branching can contribute to the neurodevelopmental pathologies associated with Fmn2 and the dynamic antagonism between Fmn2 and ADF may represent a general mechanism of formin-dependent protection of Arp2/3-initiated F-actin networks from disassembly. SIGNIFICANCE STATEMENT Axonal branching is a key process in the development of functional circuits and neural plasticity. Axon collateral branching is initiated by the elaboration of F-actin filaments from discrete axonal F-actin networks. We show that the neurodevelopmental disorder-associated formin, Fmn2, is a critical regulator of axon collateral branching. Fmn2 localizes to the collateral branch-inducing F-actin patches in axons and regulates the stability of these actin networks. The F-actin nucleation activity of Fmn2 protects the patches from ADF-mediated disassembly. Opposing activities of Fmn2 and ADF exert a dynamic regulatory control on axon collateral branch initiation and may underly the neurodevelopmental defects associated with Fmn2.

Published
2022

6. The HSPGs Syndecan and Dallylike Bind the Receptor Phosphatase LAR and Exert Distinct Effects on Synaptic Development

Author

Johnson, Karl G, Tenney, Alan P, Ghose, Aurnab, Duckworth, April M, Higashi, Misao E, Parfitt, Karen, Marcu, Oana, Heslip, Timothy R, Marsh, J Lawrence, Schwarz, Thomas L, Flanagan, John G, and Van Vactor, David

Subjects
1.1 Normal biological development and functioning, Underpinning research, Animals, Blotting, Western, Cells, Cultured, Competitive Bidding, DNA-Binding Proteins, Drosophila, Drosophila Proteins, Excitatory Postsynaptic Potentials, Growth Cones, Horseradish Peroxidase, Immunohistochemistry, Larva, Membrane Glycoproteins, Microscopy, Electron, Transmission, Models, Biological, Morphogenesis, Nerve Tissue Proteins, Neuromuscular Junction, Neurons, Phosphorylation, Protein Binding, Protein Tyrosine Phosphatases, Proteoglycans, RNA, Double-Stranded, Receptor-Like Protein Tyrosine Phosphatases, Class 2, Receptors, Cell Surface, Synapses, Synaptic Transmission, Syndecans, Transfection, Neurosciences, Psychology, Cognitive Sciences, Neurology & Neurosurgery
Abstract

The formation and plasticity of synaptic connections rely on regulatory interactions between pre- and postsynaptic cells. We show that the Drosophila heparan sulfate proteoglycans (HSPGs) Syndecan (Sdc) and Dallylike (Dlp) are synaptic proteins necessary to control distinct aspects of synaptic biology. Sdc promotes the growth of presynaptic terminals, whereas Dlp regulates active zone form and function. Both Sdc and Dlp bind at high affinity to the protein tyrosine phosphatase LAR, a conserved receptor that controls both NMJ growth and active zone morphogenesis. These data and double mutant assays showing a requirement of LAR for actions of both HSPGs lead to a model in which presynaptic LAR is under complex control, with Sdc promoting and Dlp inhibiting LAR in order to control synapse morphogenesis and function.

Published
2006

7. Molecular mechanisms mediating the induction of apoptosis by chemopreventive selenium compounds

Author

Ghose, Aurnab

Subjects
610, QR Microbiology
Abstract

Using the cervical carcinoma cell line, HeLa, molecular mediators of selenium-induced apoptosis were investigated. These studies were later extended to biopsies of normal human oral mucosa cells (NOMCs) and human oral carcinoma cells (SCCs), using a primary culture system. Two selenium compounds were tested: selenodiglutathione (SDG), the primary metabolite of selenite, the most commonly used cancer-protective selenium compound in animal models, and the synthetic compound, 1,4-phenylenebis (methylene)selenocyanate (pXSC), one of the most potent chemopreventive selenium compounds. Both compounds induced apoptosis in the cells tested and this was associated with a strong induction of Fas ligand (Fasl). Blocking Fas activation resulted in inhibition of apoptosis. Activities of stress kinases INK (c-jun N-terminal kinase) and p38 were also induced on selenium treatment and intervention studies using specific chemical inhibitors and/or dominant negative mutants suggested that INK, but not p38, was functionally important for the induction of apoptosis and Fasl. The relative levels of induction of INK activity and Fasl also correlated with the extent of apoptosis observed. On treatment with SDG, but not pXSC, SCCs were found to preferentially activate the JNK/Fasl pathway compared to NOMCs and this correlated with enhanced sensitivity of SCCs to SDG-induced apoptosis. Both SDG and pXSC also appeared to modulate activities of other signalling proteins like extracellular regulated kinases (ERKs) 1,2 & 5 and Akt. However, functional interference with these pathways using specific chemical inhibitors or constitutively activated mutants revealed either none or a small effect on apoptosis-induction. One exception was the activation of Akt by SDG in SCCs: inhibiting its activity sensitised the cells to apoptosis significantly. Finally, preliminary xenograft studies have confirmed the induction of apoptosis in vivo, using chemopreventive dietary levels of selenium.

Published
2001

9. Interim results from comparison of immune responses elicited by an inactivated and a vectored SARS-CoV-2 vaccine in seronegative and seropositive participants in India

Author

Asokan, Mangaiarkarasi, primary, Joan, Roshni Florina, additional, Babji, Sudhir, additional, Dayma, Girish, additional, Nitheesh, Prajitha, additional, Subrahmanyam, Vinutha, additional, Pandey, Archana, additional, Malagi, Girish, additional, Arya, Pooja, additional, Mahajan, Vibhuti, additional, Bhavikatti, Jayateerth, additional, Pawar, Ketakee, additional, Thorat, Aishwarya, additional, Shah, Priyanki, additional, Goud, Ramakrishna B, additional, Roy, Bishnudeo, additional, Rajukutty, Shon, additional, Immanuel, Sushil, additional, Agarwal, Dhiraj, additional, Saha, Sankhanil, additional, Shivaraj, Akshatha, additional, Panikulam, Patricia, additional, Shome, Rajeshwari, additional, Gulzar, Shah-E-Jahan, additional, Sharma, Anusmrithi U, additional, Naik, Ajinkya, additional, Talashi, Shruti, additional, Belekar, Madhuri, additional, Yadav, Ritu, additional, Khude, Poornima, additional, Mamatha, V, additional, Sudarshan, S, additional, Deshmukh, Urmila, additional, Bhise, Chinmayee, additional, Joshi, Manjiri, additional, Inbaraj, Leeberk Raja, additional, Chandrasingh, Sindhulina, additional, Ghose, Aurnab, additional, Jamora, Colin, additional, Karumbati, Anandi S, additional, Sundaramurthy, Varadharajan, additional, Johnson, Avita, additional, Ramesh, Naveen, additional, Chetan, Nirutha, additional, Parthiban, Chaitra, additional, Ahmed, Asma, additional, Rakshit, Srabanti, additional, Adiga, Vasista, additional, D’souza, George, additional, Rale, Vinay, additional, George, Carolin Elizabeth, additional, John, Jacob, additional, Kawade, Anand, additional, Chaturvedi, Akanksha, additional, Raghunathan, Anu, additional, Dias, Mary, additional, Bhosale, Anand, additional, Raghu, Padinjat, additional, Shashidhara, LS, additional, Vyakarnam, Annapurna, additional, Bal, Vineeta, additional, Kang, Gagandeep, additional, and Mayor, Satyajit, additional

Published
2023
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12. A Tale of Two Waves: Diverse Genomic and Transmission Landscapes Over 15 Months of the COVID-19 Pandemic in Pune, India

Author

Niveditha, Divya, primary, Khan, Soumen, additional, Khilari, Ajinkya, additional, Nadkarni, Sanica, additional, Bhalerao, Unnati, additional, Kadam, Pradnya, additional, Yadav, Ritu, additional, Kanekar, Jugal B, additional, Shah, Nikita, additional, Likhitkar, Bhagyashree, additional, Sawant, Rutuja, additional, Thakur, Shikha, additional, Tupekar, Manisha, additional, Nagar, Dhriti, additional, Rao, Anjani G., additional, Jagtap, Rutuja, additional, Jogi, Shraddha, additional, Belekar, Madhuri, additional, Pathak, Maitryee, additional, Shah, Priyanki, additional, Ranade, Shatakshi, additional, Phadke, Nikhil, additional, Das, Rashmita, additional, Joshi, Suvarna, additional, Karyakarte, Rajesh, additional, Ghose, Aurnab, additional, Kadoo, Narendra, additional, Shashidhara, LS, additional, Monteiro, Joy Merwin, additional, Shanmugam, Dhanasekaran, additional, Raghunathan, Anu, additional, and Karmodiya, Krishanpal, additional

Published
2022
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15. Death in Police Custody

Author

Basu, Parthiba, Gangopadhyay, Gautam, Jussy, Selvyn, Gupta, Gautam, Dasgupta, Indraneel, Dutta-Roy, Binayak, Sen, Subimal, Khasnobis, Ratan, Abrol, Dinesh, Agnihotri, Indu, Anandhi, S, Arunima, G, Bal, Bijay, Bandyopadhyay, Sudipta, Banerjee, Arindam, Banerjee, Taposik, Banerjee, Sharmistha, Baruya, Sumit Kumar, Basavaiah, Channa, Basu, Padmanava, Bhattacharya, Saumyajit, Bhattacharya, Sukanta, Bhattacharya, Sudipta, Bhattacharya, Abhijit, Bhattacharya, Dwaipayan, Bhattacharya, Jyotirmoy, Bhattacharya, Kaushik, Bhattacharya, Saswata, Bhaumik, Kamales, Bhaumik, Parthasarathi, Chakraborty, Kaberi, Chakraborty, Satyabrata, Chakraborty, Amitava, Chatterjee, Mahalaya, Chattopadhyay, Apurba Kumar, Chattopadhyay, Suchetana, Chaudhuri, Arijit, Chaudhury, Shibani, Dasgupta, Chirashree, Das, Samantak, Das, Kandarpa, Das, Surajit, Das, Jayati, Damodaran, Sumangala, Gupta, Malabika Das, Datta, Anindya, De Roy, Shantanu, Dutta, Ranjeeta, Ganguly, Sanjukta, Ghosh, Kuntal, Ghosh, Aditi, Ghose, Aurnab, Goswami, Asimananda, Haldar, Biswajit, Jana, Arun, Jana, Debnarayan, Kafi, Abdul, Kar, Guruprasad, Kesh, Dipak, Khanna, Sushil, Kidwai, Ayesha, Kundu, Anirban, Kundu, Abhijit, Mahapatra, Pradip K, Mazumdar, Shaswati, Mazumdar, Surajit, Mohanty, Mritiunjoy, Mishra, Debi Prasad, Mukhopadhyay, Ishita, Mukhopadhyay, Surajit, Nandy, Maitreyee, Pal, Amitava, Pal, Debabrata, Pal, Parthapratim, Pal, Subrata, Palriwala, Rajni, Prasad, Archana, Rajivlochan, M, Ramachandran, V K, Ray, Manas, Roy, Rahul, Sabharwal, Jyoti, Sadangi, Himansu Charan, Sarkar, Maitreyee Saha, Sarkar, Pranab, Sarkar, Sukhendu Sekhar, Sarmah, Bhupen, Sen, Sucharita, Sen, Sharmistha, Sharma, Jayeeta, Sinha, Anup, Sinha, Rajyeswar, Sreedharan, Janaky, and Vakulabharanam, Vamsi

Published
2013

24. GAPs in Slit-Robo signaling

Author

Ghose, Aurnab and Van Vactor, David

Subjects
Neurons -- Physiological aspects, Biological sciences
Published
2002

26. Community prevalence of antibodies to SARS-CoV-2 and correlates of protective immunity in an Indian metropolitan city

Author

Ghose, Aurnab, primary, Bhattacharya, Sankar, additional, Karthikeyan, Arun S., additional, Kudale, Abhay, additional, Monteiro, Joy M., additional, Joshi, Aparna, additional, Medigeshi, Guruprasad, additional, Kang, Gagandeep, additional, Bal, Vineeta, additional, Rath, Satyajit, additional, Shashidhara, L. S., additional, John, Jacob, additional, Chaudhuri, Susmita, additional, and Nagarkar, Aarti, additional

Published
2020
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40. Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth

Author

Van Vactor David, Peng Kuan-Po, Lai Tzu-Ting, Ghose Aurnab, Lee Yu-Tao, Grabbe Caroline, Kao Hsiu-Hua, Tsai Pei-I, Palmer Ruth H, Chen Ruey-Hwa, Yeh Shih-Rung, and Chien Cheng-Ting

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Focal adhesion kinase (FAK) functions in cell migration and signaling through activation of the mitogen-activated protein kinase (MAPK) signaling cascade. Neuronal function of FAK has been suggested to control axonal branching; however, the underlying mechanism in this process is not clear. Results We have generated mutants for the Drosophila FAK gene, Fak56. Null Fak56 mutants display overgrowth of larval neuromuscular junctions (NMJs). Localization of phospho-FAK and rescue experiments suggest that Fak56 is required in presynapses to restrict NMJ growth. Genetic analyses imply that FAK mediates the signaling pathway of the integrin αPS3βν heterodimer and functions redundantly with Src. At NMJs, Fak56 downregulates ERK activity, as shown by diphospho-ERK accumulation in Fak56 mutants, and suppression of Fak56 mutant NMJ phenotypes by reducing ERK activity. Conclusion We conclude that Fak56 is required to restrict NMJ growth during NMJ development. Fak56 mediates an extracellular signal through the integrin receptor. Unlike its conventional role in activating MAPK/ERK, Fak56 suppresses ERK activation in this process. These results suggest that Fak56 mediates a specific neuronal signaling pathway distinct from that in other cellular processes.

Published
2008
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48. Fak56 functions downstream of integrin alphaPS3betanu and suppresses MAPK activation in neuromuscular junction growth.

Author

Tsai, Pei-I, Kao, Hsiu-Hua, Grabbe, Caroline, Lee, Yu-Tao, Ghose, Aurnab, Lai, Tzu-Ting, Peng, Kuan-Po, Van Vactor, David, Palmer, Ruth H, Chen, Ruey-Hwa, Yeh, Shih-Rung, Chien, Cheng-Ting, Tsai, Pei-I, Kao, Hsiu-Hua, Grabbe, Caroline, Lee, Yu-Tao, Ghose, Aurnab, Lai, Tzu-Ting, Peng, Kuan-Po, Van Vactor, David, Palmer, Ruth H, Chen, Ruey-Hwa, Yeh, Shih-Rung, and Chien, Cheng-Ting

Abstract

BACKGROUND: Focal adhesion kinase (FAK) functions in cell migration and signaling through activation of the mitogen-activated protein kinase (MAPK) signaling cascade. Neuronal function of FAK has been suggested to control axonal branching; however, the underlying mechanism in this process is not clear. RESULTS: We have generated mutants for the Drosophila FAK gene, Fak56. Null Fak56 mutants display overgrowth of larval neuromuscular junctions (NMJs). Localization of phospho-FAK and rescue experiments suggest that Fak56 is required in presynapses to restrict NMJ growth. Genetic analyses imply that FAK mediates the signaling pathway of the integrin alphaPS3betanu heterodimer and functions redundantly with Src. At NMJs, Fak56 downregulates ERK activity, as shown by diphospho-ERK accumulation in Fak56 mutants, and suppression of Fak56 mutant NMJ phenotypes by reducing ERK activity. CONCLUSION: We conclude that Fak56 is required to restrict NMJ growth during NMJ development. Fak56 mediates an extracellular signal through the integrin receptor. Unlike its conventional role in activating MAPK/ERK, Fak56 suppresses ERK activation in this process. These results suggest that Fak56 mediates a specific neuronal signaling pathway distinct from that in other cellular processes.

Published
2008
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49. Formin 2 regulates the stabilization of filopodial tip adhesions in growth cones and affects neuronal outgrowth and pathfinding in vivo.

Author

Sahasrabudhe, Abhishek, Ghate, Ketakee, Mutalik, Sampada, Jacob, Ajesh, and Ghose, Aurnab

Subjects
FILOPODIA, CHEMICAL senses, SPINAL cord, FIBROBLASTS, NEURONS
Abstract

Growth cone filopodia are actin-based mechanosensory structures that are essential for chemoreception and the generation of contractile forces necessary for directional motility. However, little is known about the influence of filopodial actin structures on substrate adhesion and filopodial contractility. Formin 2 (Fmn2) localizes along filopodial actin bundles and its depletion does not affect filopodia initiation or elongation. However, Fmn2 activity is required for filopodial tip adhesion maturation and the ability of filopodia to generate traction forces. Dysregulation of filopodia in Fmn2-depleted neurons leads to compromised growth cone motility. Additionally, in mouse fibroblasts, Fmn2 regulates ventral stress fiber assembly and affects the stability of focal adhesions. In the developing chick spinal cord, Fmn2 activity is required cellautonomously for the outgrowth and pathfinding of spinal commissural neurons. Our results reveal an unanticipated function for Fmn2 in neural development. Fmn2 regulates structurally diverse bundled actin structures, parallel filopodial bundles in growth cones and anti-parallel stress fibers in fibroblasts, in turn modulating the stability of substrate adhesions. We propose Fmn2 as a mediator of actin bundle integrity, enabling efficient force transmission to the adhesion sites. [ABSTRACT FROM AUTHOR]

Published
2016
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50. Mottled Mice and Non-Mammalian Models of Menkes Disease.

Author

Lenartowicz, Małgorzata, Krzeptowski, Wojciech, Lipiński, Paweł, Grzmil, Paweł, Starzyński, Rafał, Pierzchała, Olga, Møller, Lisbeth Birk, Ghose, Aurnab, and Padinjat, Raghu

Subjects
KINKY hair syndrome, LABORATORY mice
Abstract

Menkes disease is a multi-systemic copper metabolism disorder caused by mutations in the X-linked ATP7A gene and characterized by progressive neurodegeneration and severe connective tissue defects. The ATP7A protein is a copper (Cu)-transporting ATPase expressed in all tissues and plays a critical role in the maintenance of copper homeostasis in cells of the whole body. ATP7A participates in copper absorption in the small intestine and in copper transport to the central nervous system (CNS) across the blood-brain-barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB). Cu is essential for synaptogenesis and axonal development. In cells, ATP7A participates in the incorporation of copper into Cu-dependent enzymes during the course of its maturation in the secretory pathway. There is a high degree of homology (>80%) between the human ATP7A and murine Atp7a genes. Mice with mutations in the Atp7a gene, called mottled mutants, are well-established and excellent models of Menkes disease. Mottled mutants closely recapitulate the Menkes phenotype and are invaluable for studying Cumetabolism. They provide useful models for exploring and testing new forms of therapy in Menkes disease. Recently, non-mammalian models of Menkes disease, Drosophila melanogaster and Danio rerio mutants were used in experiments which would be technically difficult to carry out in mammals. [ABSTRACT FROM AUTHOR]

Published
2015
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