View Item 

Show simple item record

Neural deletion of Sh2b1 results in brain growth retardation and reactive aggression
dc.contributor.authorJiang, Lin
dc.contributor.authorSu, Haoran
dc.contributor.authorKeogh, Julia M.
dc.contributor.authorChen, Zheng
dc.contributor.authorHenning, Elana
dc.contributor.authorWilkinson, Paul
dc.contributor.authorGoodyer, Ian
dc.contributor.authorFarooqi, I. Sadaf
dc.contributor.authorRui, Liangyou
dc.date.accessioned2020-04-02T18:40:16Z
dc.date.available2020-04-02T18:40:16Z
dc.date.issued2018-04
dc.identifier.citationJiang, Lin; Su, Haoran; Keogh, Julia M.; Chen, Zheng; Henning, Elana; Wilkinson, Paul; Goodyer, Ian; Farooqi, I. Sadaf; Rui, Liangyou (2018). "Neural deletion of Sh2b1 results in brain growth retardation and reactive aggression." The FASEB Journal 32(4): 1830-1840.
dc.identifier.issn0892-6638
dc.identifier.issn1530-6860
dc.identifier.urihttps://hdl.handle.net/2027.42/154676
dc.publisherWiley Periodicals, Inc.
dc.publisherFederation of American Societies for Experimental Biology
dc.subject.otherbrain development
dc.subject.otherBDNF
dc.subject.otheraggression circuits
dc.titleNeural deletion of Sh2b1 results in brain growth retardation and reactive aggression
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelBiology
dc.subject.hlbtoplevelScience
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttps://deepblue.lib.umich.edu/bitstream/2027.42/154676/1/fsb2fj201700831r.pdf
dc.identifier.doi10.1096/fj.201700831R
dc.identifier.sourceThe FASEB Journal
dc.identifier.citedreferenceStowers, L., Cameron, P., and Keller, J. A. ( 2013 ) Ominous odors: olfactory control of instinctive fear and aggression in mice. Curr. Opin. Neurobiol. 23, 339 – 345
dc.identifier.citedreferenceNiv, S., Tuvblad, C., Raine, A., and Baker, L. A. ( 2013 ) Aggression and rule‐breaking. heritability and stability of antisocial behavior problems in childhood and adolescence. J. Crim. Justice 41
dc.identifier.citedreferenceDavidson, R. J., Putnam, K. M., and Larson, C. L. ( 2000 ) Dysfunction in the neural circuitry of emotion regulation—a possible prelude to violence. Science 289, 591 – 594
dc.identifier.citedreferenceBrunner, H. G., Nelen, M., Breakefield, X. O., Ropers, H. H., and van Oost, B. A. ( 1993 ) Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Science 262, 578 – 580
dc.identifier.citedreferenceBevilacqua, L., Doly, S., Kaprio, J., Yuan, Q., Tikkanen, R., Paunio, T., Zhou, Z., Wedenoja, J., Maroteaux, L., Diaz, S., Belmer, A., Hodgkinson, C. A., Dell’osso, L., Suvisaari, J., Coccaro, E., Rose, R. J., Peltonen, L., Virkkunen, M., and Goldman, D. ( 2010 ) A population‐specific HTR2B stop codon predisposes to severe impulsivity. Nature 468, 1061 – 1066
dc.identifier.citedreferenceRui, L. ( 2014 ) SH2B1 regulation of energy balance, body weight, and glucose metabolism. World J. Diabetes 5, 511 – 526
dc.identifier.citedreferenceRen, D., Li, M., Duan, C., and Rui, L. ( 2005 ) Identification of SH2‐B as a key regulator of leptin sensitivity, energy balance, and body weight in mice. Cell Metab. 2, 95 – 104
dc.identifier.citedreferenceRios, M. ( 2014 ) Neurotrophins and the regulation of energy balance and body weight. Handb. Exp. Pharmacol. 220, 283 – 307
dc.identifier.citedreferenceXu, B., Goulding, E. H., Zang, K., Cepoi, D., Cone, R. D., Jones, K. R., Tecott, L. H., and Reichardt, L. F. ( 2003 ) Brain‐derived neurotrophic factor regulates energy balance downstream of melanocortin‐4 receptor. Nat. Neurosci. 6, 736 – 742
dc.identifier.citedreferenceRen, D., Zhou, Y., Morris, D., Li, M., Li, Z., and Rui, L. ( 2007 ) Neuronal SH2B1 is essential for controlling energy and glucose homeostasis. J. Clin. Invest. 117, 397 – 406
dc.identifier.citedreferenceBochukova, E. G., Huang, N., Keogh, J., Henning, E., Purmann, C., Blaszczyk, K., Saeed, S., Hamilton‐Shield, J., Clayton‐Smith, J., O’Rahilly, S., Hurles, M. E., and Farooqi, I. S. ( 2010 ) Large, rare chromosomal deletions associated with severe early‐onset obesity. Nature 463, 666 – 670
dc.identifier.citedreferenceDoche, M. E., Bochukova, E. G., Su, H. W., Pearce, L. R., Keogh, J. M., Henning, E., Cline, J. M., Saeed, S., Dale, A., Cheetham, T., Barroso, I., Argetsinger, L. S., O’Rahilly, S., Rui, L., Carter‐Su, C., and Farooqi, I. S. ( 2012 ) Human SH2B1 mutations are associated with maladaptive behaviors and obesity. J. Clin. Invest. 122, 4732 – 4736; erratum: 123, 526
dc.identifier.citedreferencePearce, L. R., Joe, R., Doche, M. E., Su, H. W., Keogh, J. M., Henning, E., Argetsinger, L. S., Bochukova, E. G., Cline, J. M., Garg, S., Saeed, S., Shoelson, S., O’Rahilly, S., Barroso, I., Rui, L., Farooqi, I. S., and Carter‐Su, C. ( 2014 ) Functional characterization of obesity‐associated variants involving the α and β isoforms of human SH2B1. Endocrinology 155, 3219 – 3226
dc.identifier.citedreferenceChen, Z., Morris, D. L. Jiang, L., Liu, Y., and Rui, L. ( 2014 ) SH2B1 in β‐cells regulates glucose metabolism by promoting β‐cell survival and islet expansion. Diabetes 63, 585 – 595
dc.identifier.citedreferenceSclafani, A. M., Skidmore, J. M., Ramaprakash, H., Trumpp, A., Gage, P. J., and Martin, D. M. ( 2006 ) Nestin‐Cre mediated deletion of Pitx2 in the mouse. Genesis 44, 336 – 344
dc.identifier.citedreferenceHegedus, B., Dasgupta, B., Shin, J. E., Emnett, R. J., Hart‐Mahon, E. K., Elghazi, L., Bernal‐Mizrachi, E., and Gutmann, D. H. ( 2007 ) Neurofibromatosis‐1 regulates neuronal and glial cell differentiation from neuroglial progenitors in vivo by both cAMP‐ and Rasdependent mechanisms. Cell Stem Cell 1, 443 – 457
dc.identifier.citedreferenceStowers, L., Holy, T. E., Meister, M., Dulac, C., and Koentges, G. ( 2002 ) Loss of sex discrimination and male‐male aggression in mice deficient for TRP2. Science 295, 1493 – 1500
dc.identifier.citedreferenceLyons, W. E., Mamounas, L. A., Ricaurte, G. A., Coppola, V., Reid, S. W., Bora, S. H., Wihler, C., Koliatsos, V. E., and Tessarollo, L. ( 1999 ) Brain‐derived neurotrophic factor‐deficient mice develop aggressiveness and hyperphagia in conjunction with brain serotonergic abnormalities. Proc. Natl. Acad. Sci. USA 96, 15239 – 15244
dc.identifier.citedreferenceIto, W., Chehab, M., Thakur, S., Li, J., and Morozov, A. ( 2011 ) BDNF‐restricted knockout mice as an animal model for aggression. Genes Brain Behav. 10, 365 – 374
dc.identifier.citedreferenceChan, J. P., Unger, T. J., Byrnes, J., and Rios, M. ( 2006 ) Examination of behavioral deficits triggered by targeting Bdnf in fetal or postnatal brains of mice. Neuroscience 142, 49 – 58
dc.identifier.citedreferenceQian, X., Riccio, A., Zhang, Y., and Ginty, D. D. ( 1998 ) Identification and characterization of novel substrates of Trk receptors in developing neurons. Neuron 21, 1017 – 1029
dc.identifier.citedreferenceVilar, M., and Mira, H. ( 2016 ) Regulation of neurogenesis by neurotrophins during adulthood: expected and unexpected roles. Front. Neurosci. 10, 26
dc.identifier.citedreferencePark, H., and Poo, M. M. ( 2013 ) Neurotrophin regulation of neural circuit development and function. Nat. Rev. Neurosci. 14, 7 – 23
dc.identifier.citedreferenceRui, L., Herrington, J., and Carter‐Su, C. ( 1999 ) SH2‐B is required for nerve growth factor‐induced neuronal differentiation. J. Biol. Chem. 274, 10590 – 10594
dc.identifier.citedreferenceShih, C. H., Chen, C. J., and Chen, L. ( 2013 ) New function of the adaptor protein SH2B1 in brain‐derived neurotrophic factor‐induced neurite outgrowth. PLoS One 8, e79619
dc.identifier.citedreferenceRios, M., Fan, G., Fekete, C., Kelly, J., Bates, B., Kuehn, R., Lechan, R. M., and Jaenisch, R. ( 2001 ) Conditional deletion of brain‐derived neurotrophic factor in the postnatal brain leads to obesity and hyperactivity. Mol. Endocrinol. 15, 1748 – 1757
dc.identifier.citedreferenceNelson, R. J., and Trainor, B. C. ( 2007 ) Neural mechanisms of aggression. Nat. Rev. Neurosci. 8, 536 – 546
dc.identifier.citedreferenceBarr, C. S., and Driscoll, C. ( 2014 ) Neurogenetics of aggressive behavior. studies in primates. Curr. Top. Behav. Neurosci. 17, 45 – 71
dc.identifier.citedreferenceDorfman, H. M., Meyer‐Lindenberg, A., and Buckholtz, J. W. ( 2014 ) Neurobiological mechanisms for impulsive‐aggression. the role of MAOA. Curr. Top. Behav. Neurosci. 17, 297 – 313
dc.identifier.citedreferenceHong, W., Kim, D. W., and Anderson, D. J. ( 2014 ) Antagonistic control of social versus repetitive self‐grooming behaviors by separable amygdala neuronal subsets. Cell 158, 1348 – 1361
dc.identifier.citedreferenceAnderson, D. J. ( 2012 ) Optogenetics, sex, and violence in the brain. implications for psychiatry. Biol. Psychiatry 71, 1081 – 1089
dc.identifier.citedreferenceTakahashi, A., and Miczek, K. A. ( 2014 ) Neurogenetics of aggressive behavior. studies in rodents. Curr. Top. Behav. Neurosci. 17, 3 – 44
dc.identifier.citedreferenceGregg, T. R., and Siegel, A. ( 2001 ) Brain structures and neurotransmitters regulating aggression in cats. implications for human aggression. Prog. Neuropsychopharmacol. Biol. Psychiatry 25, 91 – 140
dc.identifier.citedreferenceLin, D., Boyle, M. P., Dollar, P., Lee, H., Lein, E. S., Perona, P., and Anderson, D. J. ( 2011 ) Functional identification of an aggression locus in the mouse hypothalamus. Nature 470, 221 – 226
dc.identifier.citedreferenceBlair, R. J. ( 2007 ) Aggression, psychopathy and free will from a cognitive neuroscience perspective. Behav. Sci. Law 25, 321 – 331
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
fsb2fj201700831r.pdf
Size:
1.954MB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.