Marisa Jackson

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==Contact Info==
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[[Image:MJ_smile.jpg|thumb|right|upright=.75|This is me. Hi!]]
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*Marisa Jackson
 
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*Northwestern University
 
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*303 E. Chicago Ave.
 
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*Ward Building, 7-011
 
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*Chicago, IL 60611
 
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*[[Special:Emailuser/Marisa Jackson|Email me through OpenWetWare]]
 
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I'm an MSTP student in the [[Tourtellotte Lab]] at Northwestern University. I'm currently studying the role of IKAP in the development and maintenance of the sympathetic nervous system. IKAP is believed to be a part of the Elongator complex, which has been implicated in histone and, more recently, α-tubulin acetylation. A point mutation leading to the variable, premature truncation of this protein has been linked to familial dysautonomia, type 3 of the hereditary sensory and autonomic neuropathies (HSANs). This mutation is present in >99.5% of cases. While the causative mutation is present in all cells (and the protein is ubiquitously expressed), the abnormal splicing occurs preferentially within the nervous system.  All 5 of the HSANs manifest with sensory deficits and varying degrees of autonomic dysfunction, familial dysautonomia being the most common. The disease is associated with a range of severe symptoms, including impaired pain/temperature sensation, postural hypotension, episodic vomiting and scoliosis.
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<font size="4">Marisa Jackson</font size>
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We are currently generating a conditional knockout (cKO) mouse model of familial dysautonomia that will allow us to investigate the ''in vivo'' consequences of Ikap depletion.
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<font size="2">Department of Pathology<br>
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303 E. Chicago Ave.<br>
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Ward Building, 7-011<br>
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Chicago, IL 60611<br>
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==Education==
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Email: marisa-jackson@md.northwestern.edu
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<!--Include info about your educational background-->
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* 2005, BA, Washington University in St. Louis
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==Research interests==
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# Neuropathology
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I’m an MSTP student in the Tourtellotte Lab at Northwestern University. I'm currently studying the role of IKAP in the development and maintenance of the sympathetic nervous system. IKAP is believed to be a part of the Elongator complex, which has been implicated in histone and, more recently, α-tubulin acetylation. A point mutation leading to the variable, premature truncation of this protein has been linked to familial dysautonomia, type 3 of the hereditary sensory and autonomic neuropathies (HSANs). This mutation is present in >99.5% of cases. While the causative mutation is present in all cells (and the protein is ubiquitously expressed), the abnormal splicing occurs preferentially within the nervous system. All 5 of the HSANs manifest with sensory deficits and varying degrees of autonomic dysfunction, familial dysautonomia being the most common. The disease is associated with a range of severe symptoms, including impaired pain/temperature sensation, postural hypotension, episodic vomiting and scoliosis.
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# Molecular biology
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We are currently generating a conditional knockout (cKO) mouse model of familial dysautonomia that will allow us to investigate the in vivo consequences of Ikap depletion.
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# Neurodevelopment
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==Publications==
 
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<!-- Replace the PubMed ID's ("pmid=#######") below with the PubMed ID's for your publications.  You can add or remove lines as needed -->
 
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Coming soon...
 
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==Favorite Links==
 
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[http://www.northwestern.edu Northwestern University]
 
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[http://www.huffingtonpost.com Huffington Post]
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== Research Interests ==
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<blockquote>
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*Neuropathology
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*Molecular Biology
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*Neurodevelopment
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</blockquote>
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== Education==
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<blockquote>B.A in Biology, 2005, Washington University in St. Louis <br>
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<br>
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</blockquote>
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== Publications ==
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<blockquote>Coming soon...
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<br>

Revision as of 12:37, 19 May 2010


Marisa Jackson

Department of Pathology
303 E. Chicago Ave.
Ward Building, 7-011
Chicago, IL 60611

Email: marisa-jackson@md.northwestern.edu

I’m an MSTP student in the Tourtellotte Lab at Northwestern University. I'm currently studying the role of IKAP in the development and maintenance of the sympathetic nervous system. IKAP is believed to be a part of the Elongator complex, which has been implicated in histone and, more recently, α-tubulin acetylation. A point mutation leading to the variable, premature truncation of this protein has been linked to familial dysautonomia, type 3 of the hereditary sensory and autonomic neuropathies (HSANs). This mutation is present in >99.5% of cases. While the causative mutation is present in all cells (and the protein is ubiquitously expressed), the abnormal splicing occurs preferentially within the nervous system. All 5 of the HSANs manifest with sensory deficits and varying degrees of autonomic dysfunction, familial dysautonomia being the most common. The disease is associated with a range of severe symptoms, including impaired pain/temperature sensation, postural hypotension, episodic vomiting and scoliosis. We are currently generating a conditional knockout (cKO) mouse model of familial dysautonomia that will allow us to investigate the in vivo consequences of Ikap depletion.


Research Interests

  • Neuropathology
  • Molecular Biology
  • Neurodevelopment

Education

B.A in Biology, 2005, Washington University in St. Louis

Publications

Coming soon...
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