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6. Marginal zone B cells acquire dendritic cell functions by trogocytosis

Author

Schriek, Patrick, primary, Ching, Alan C., additional, Moily, Nagaraj S., additional, Moffat, Jessica, additional, Beattie, Lynette, additional, Steiner, Thiago M., additional, Hosking, Laine M., additional, Thurman, Joshua M., additional, Holers, V. Michael, additional, Ishido, Satoshi, additional, Lahoud, Mireille H., additional, Caminschi, Irina, additional, Heath, William R., additional, Mintern, Justine D., additional, and Villadangos, Jose A., additional

Published
2022
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12. Summaries of oral sessions at the XXI World Congress of Psychiatric Genetics, Boston, Massachusetts, 17–21 October 2013

Author

Akpudo, Hilary, Aleksic, Branko, Alkelai, Anna, Burton, Christie, Carrillo-Roa, Tania, Carillo Roa, Tania, Chen, David T W, Cheng, Min-Chih, Cocchi, Enrico, Davis, Lea K, Giori, Isabele G, Hubbard, Leon M, Merikangas, Alison, Moily, Nagaraj S, Okewole, Adeniran, Olfson, Emily, Pappa, Irene, Reitt, Markus, Singh, Ajeet B, Steinberg, Julia, Strohmaier, Jana, Ting, Te-Tien, van Hulzen, Kimm J E, O'Shea, Anne, DeLisi, Lynn E, Clinical Child and Family Studies, and Department of Psychology, Education and Child Studies

Subjects
medicine.medical_specialty, Mutation/genetics, Endophenotypes, media_common.quotation_subject, Statistics as Topic, Library science, Biomarkers/metabolism, State (polity), Genetics, medicine, Humans, Gene Regulatory Networks, Genetic Testing, Nicotine dependence, Psychiatry, Biological Psychiatry, Genetics (clinical), Psychiatric genetics, media_common, Mental Disorders/genetics, Stem Cells/metabolism, Genomics, medicine.disease, Psychiatry and Mental health, Neurodevelopmental disorders Radboud Institute for Molecular Life Sciences [Radboudumc 7], Psychology, Boston, Genome-Wide Association Study
Abstract

Item does not contain fulltext The XXI World Congress of Psychiatric Genetics (WCPG), sponsored by the International Society of Psychiatric Genetics (ISPG), took place in Boston, Massachusetts, on 17-21 October 2013. Approximately 900 participants gathered to discuss the latest findings in this rapidly advancing field. The following report was written by student travel awardees. Each was assigned one or more sessions as a rapporteur. This manuscript represents topics covered in most, but not all of the oral presentations during the conference, and contains some of the major notable new findings reported.

Published
2014

13. A linkage and exome study implicates rare variants of KANK4 and CAP2 in bipolar disorder in a multiplex family.

Author

Anjanappa, Ram M., Nayak, Sourav, Moily, Nagaraj S., Manduva, Vallikiran, Nadella, Ravi K., Viswanath, Biju, Reddy, Yemmiganur C. J., Jain, Sanjeev, and Anand, Anuranjan

Subjects
BIPOLAR disorder, GENETIC markers, NEUROBEHAVIORAL disorders, GENETIC disorders, FAMILIES
Abstract

Objectives: Bipolar disorder (BD) is a neuropsychiatric disorder with a complex pattern of inheritance. Although many genetic studies have been conducted on BD, its genetic correlates remain uncertain. This study was aimed at identifying the genetic underpinnings of the disorder in an Indian family, which has been under comprehensive clinical evaluation and follow‐up for over 12 years. Methods: We analysed a four‐generation family with several of its members diagnosed for BD employing a combination of genetic linkage and exome analysis. Results: We obtained suggestive LOD score for a chromosome 1 and a chromosome 6 marker (D1S410; LOD = 3.01, Ө = 0; and D6S289; LOD = 1.58, Ө = 0). Manual haplotyping of the regions encompassing these two markers helped delimit a critical genomic interval of 32.44 Mb (D1S2700‐D1S435; chromosome 1p31.1‐13.2) and another of 10.34 Mb (D6S470‐D6S422; chromosome 6p22.3‐22.2). We examined the exomic sequences corresponding to these two intervals and found rare variants, NM_181712.4: c.2461G>T (p.Asp821Tyr) in KANK4 at 1p31.1‐13.2; and NM_006366:c.‐93G>A, in the 5' UTR of CAP2 at 6p22.3‐22.2. Conclusions: Our studysuggests involvement of KANK4 or CAP2 or both in BD in this family. Further analysis of these two genes in BD patients and functional evaluation of the allelic variants identified are suggested. [ABSTRACT FROM AUTHOR]

Published
2020
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14. A Thiol Probe for Measuring Unfolded Protein Load and Proteostasis in Cells

Author

Chen, Moore Z., Moily, Nagaraj S., Bridgford, Jessica L., Wood, Rebecca J., Radwan, Mona, Smith, Trevor A., Song, Zhegang, Tang, Ben Zhong, Tilley, Leann, Xu, Xiaohong, Reid, Gavin E., Pouladi, Mahmoud A., Hong, Yuning, Hatters, Danny M., Chen, Moore Z., Moily, Nagaraj S., Bridgford, Jessica L., Wood, Rebecca J., Radwan, Mona, Smith, Trevor A., Song, Zhegang, Tang, Ben Zhong, Tilley, Leann, Xu, Xiaohong, Reid, Gavin E., Pouladi, Mahmoud A., Hong, Yuning, and Hatters, Danny M.

Abstract

When proteostasis becomes unbalanced, unfolded proteins can accumulate and aggregate. Here we report that the dye, tetraphenylethene maleimide (TPE-MI) can be used to measure cellular unfolded protein load. TPE-MI fluorescence is activated upon labelling free cysteine thiols, normally buried in the core of globular proteins that are exposed upon unfolding. Crucially TPE-MI does not become fluorescent when conjugated to soluble glutathione. We find that TPE-MI fluorescence is enhanced upon reaction with cellular proteomes under conditions promoting accumulation of unfolded proteins. TPE-MI reactivity can be used to track which proteins expose more cysteine residues under stress through proteomic analysis. We show that TPE-MI can report imbalances in proteostasis in induced pluripotent stem cell models of Huntington disease, as well as cells transfected with mutant Huntington exon 1 before the formation of visible aggregates. TPE-MI also detects protein damage following dihydroartemisinin treatment of the malaria parasites Plasmodium falciparum. TPE-MI therefore holds promise as a tool to probe proteostasis mechanisms in disease. © 2017 The Author(s).

Published
2017

15. A thiol probe for measuring unfolded protein load and proteostasis in cells

Author

Chen, Moore Z., primary, Moily, Nagaraj S., additional, Bridgford, Jessica L., additional, Wood, Rebecca J., additional, Radwan, Mona, additional, Smith, Trevor A., additional, Song, Zhegang, additional, Tang, Ben Zhong, additional, Tilley, Leann, additional, Xu, Xiaohong, additional, Reid, Gavin E., additional, Pouladi, Mahmoud A., additional, Hong, Yuning, additional, and Hatters, Danny M., additional

Published
2017
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16. Huntingtin Inclusions Trigger Cellular Quiescence, Deactivate Apoptosis, and Lead to Delayed Necrosis

Author

Ramdzan, Yasmin M., primary, Trubetskov, Mikhail M., additional, Ormsby, Angelique R., additional, Newcombe, Estella A., additional, Sui, Xiaojing, additional, Tobin, Mark J., additional, Bongiovanni, Marie N., additional, Gras, Sally L., additional, Dewson, Grant, additional, Miller, Jason M.L., additional, Finkbeiner, Steven, additional, Moily, Nagaraj S., additional, Niclis, Jonathan, additional, Parish, Clare L., additional, Purcell, Anthony W., additional, Baker, Michael J., additional, Wilce, Jacqueline A., additional, Waris, Saboora, additional, Stojanovski, Diana, additional, Böcking, Till, additional, Ang, Ching-Seng, additional, Ascher, David B., additional, Reid, Gavin E., additional, and Hatters, Danny M., additional

Published
2017
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20. Association of GRIN1, ABCB1, and DRD4 genes and response to antipsychotic drug treatment in schizophrenia

Author

Pai, Pranita, primary, Arathil, Praveen, additional, Kotambail, Ananthapadmanabha, additional, Nair, Rajesh, additional, Gupta, Meenal, additional, Moily, Nagaraj S., additional, Kukreti, Ritushree, additional, Jain, Sanjeev, additional, Rai, Padmalatha S., additional, Gopinath, Puthiya M., additional, Sharma, Podila S., additional, and Satyamoorthy, Kapaettu, additional

Published
2015
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25. Off label use of lithium in the treatment of Huntington's disease: A case series.

Author

Danivas, Vijay, Moily, Nagaraj S., Thimmaiah, Rohini, Muralidharan, Kesavan, Purushotham, Meera, Muthane, Uday, and Jain, Sanjeev

Subjects
*THERAPEUTIC use of lithium, *CHOREA, *AFFECT (Psychology), *HUNTINGTON disease, *LITHIUM, *HEALTH outcome assessment, *BODY movement, *TREATMENT effectiveness, *OFF-label use (Drugs), *PREVENTION, *GENETICS
Abstract

Huntington's disease is characterized by choreic movements, psychiatric disorders, striatal atrophy with selective small neuronal loss, and autosomal dominant inheritance. The genetic abnormality is CAG expansion in Huntingtin gene. Newer therapeutic strategies are evolving to treat this progressive disorder. The neuroprotective agents are one such group of drugs being tried. Lithium has been used to treat Huntington's disease in the past due to its neuroprotective effects. Though the precise mechanism of action is not clear, Lithium can directly or indirectly modulate proteins involved in neuronal survival/differentiation which may account for its neuroprotective effects. We report three patients with Huntington's disease in whom Lithium prevented the progression of chorea and also helped stabilize mood. [ABSTRACT FROM AUTHOR]

Published
2013
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