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Journal of Postdoctoral Research (JPR) - Vol. 2 No. 6 June 2014
Targeting Interleukin-2-Inducible T-cell Kinase (ITK) in T-Cell Related Diseases
Yiming Zhong, Amy J. Johnson, John C. Byrd, and Jason A. Dubovsky

Involvement of endoplasmic reticulum stress in TDP-43-linked neurodegenerative disease
Adam K. Walker


Modulation of Olfactory Receptor Neuron Sensitivity by Hunger in Drosophila
De-Shou Cao, Tuhin Subhra Chakraborty, Neeraj Soni, and Pallavi Rao Netrakanti




Tie1, The Orphan Receptor No Longer in the Shadows
Nikolett M. Biel


Ubiquilin-1 Augments Recovery from Cerebral Ischemia
Anand krishnan


Supporting the NIH: the Original Crowdfunding of Medical Research
Stephan C. Jahn


Postdoctoral Research Grants Writing: Moving A Step Ahead
Ehtesham Arif


A Postdoc’s Guide to Being a Postdoc
Stefanie B. Marquez


Author(s)
Yiming Zhong, Amy J. Johnson, John C. Byrd, and Jason A. Dubovsky
Address
Division of Hematology, Department of Internal Medicine, OSU, 320 W. 10th Avenue, Columbus, OH 43210, USA
Abstract:

IL2-inducible T-cell kinase (ITK), a member of the Tec family tyrosine kinases, is the predominant Tec kinase in T cells and natural killer (NK) cells mediating T cell receptor (TCR) and Fc receptor (Fc R) initiated signal transduction. ITK deficiency results in impaired T and NK cell functions, leading to various disorders including malignancies, inflammation, and autoimmune diseases. In this mini-review, the role of ITK in Tcell signaling and the development of small molecule inhibitors of ITK for the treatment of T-cell related disorders is examined.


Author(s)
Adam K. Walker

Address
Center for Neurodegenerative Disease Research, Perelman School of Medicine, UPenn, Philadelphia, Pennsylvania 19104, USA
Abstract:

Phosphorylated and ubiquitinated TAR DNA binding protein 43 (TDP-43) pathology is the neurodegenerative hallmark of the vast majority of amyotrophic lateral sclerosis (ALS) and approximately half of all frontotemporal lobar degeneration (FTLD) cases. An RNA/DNA-binding protein with diverse roles in the nucleus, TDP-43 accumulates in the cytoplasm of affected neurons and glia in disease, indicating that both a loss of normal nuclear function and additional gain of toxicity due to increased cytoplasmic presence likely occur in these TDP-43 proteinopathies. Abundance and splicing of hundreds of transcripts are affected by dysfunction of TDP-43, making identification of the key pathways involved in disease pathogenesis a difficult task. However, endoplasmic reticulum (ER) stress and activation of the unfolded protein response have been described in sporadic ALS patient tissues as well as in cell and animals models of widely-studied superoxide dismutase 1 (SOD1) mutation-linked ALS. These responses to misfolded proteins have more recently been demonstrated in models of TDP-43-linked disease, and modulation of ER stress, which is intimately associated with oxidative stress and formation of stress granules in cells, could therefore represent one avenue for potential amelioration of ALS and FTLD. This review summarizes recent findings describing the involvement of ER stress in TDP-43 proteinopathies.


Author(s)
De-Shou Cao, Tuhin Subhra Chakraborty, Neeraj Soni, and Pallavi Rao Netrakanti



Address
UCSD, USA ; U Copenhagen, Denmark ; TIFR, Bangalore, India.
Abstract:

Hunger drives animals to search for food, a behavior that is heavily dependent on the olfactory system. The neuronal mechanism by which hunger modulates the behavioral response towards food odor, however, is not well understood. In this study, using a single-fly behavioral assay and single-unit recording, we have demonstrated that starved flies exhibit enhanced attraction towards an attractive odor, ethyl acetate, via increased sensitization of the olfactory receptor neurons (ORNs). These results suggest that the increased attraction behavior caused by hunger is due to enhanced sensitivity in the ORNs.


Author(s)
Nikolett M. Biel

Address
Department of Pathology, University of Florida College of Medicine, Gainesville, FL 32610, USA
Abstract:

Angiogenesis, the formation of new blood vessels from pre-existing ones, occurs during physiological conditions such as wound healing, pregnancy and the menstrual cycle. It is also a fundamental process in pathological conditions such as tumor development, ocular disease, diabetes, atherosclerosis and arthritis. Angiogenesis as a therapeutic target (especially Vascular Endothelial Growth Factor (VEGF) inhibitors) has been heavily pursued in numerous cancer settings with promising results yet fallen short of its expectations. The discovery of the endothelial cell specific Angiopoietin/Tie axis and its role in normal and pathological angiogenesis led to the development of second-generation anti-angiogenic agents. Most of the effort has been to target the pro-angiogenic factor Ang-2 and its receptor Tie2. The present research highlight focuses on a study by D’Amico et al.,.....


Author(s)
Anand krishnan

Address

Department of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, AB, T2N 4C2, Canada

Abstract:

Excess production and actions of reactive oxygen species (ROS) is a major trigger for the progression of molecular abnormalities that accompany many diseases. For example, cerebral ischemia-mediated surge of ROS induce misfolding and microaggregation of proteins resulting in protein dysfunction and toxicity in the affected areas. Timely removal of the ROS inducers and dysfunctional proteins may be an ideal strategy to prevent the complications caused by the ROS. A recent article published byLiu and colleagues demonstrated that ubiquilin-1 (Ubqln), an ubiquitin-like protein,prevents ROS mediated complications in cerebral ischemia. Ubqln mediated timely degradation of dysfunctional proteins is sought to mediate this protective effect.


Author(s)
Stephan C. Jahn

Address
Department of Medicinal Chemistry and UF Health Cancer Center, University of Florida, Gainesville, FL 32610, USA
Abstract:

There is strong support in our society for increased medical research and Americans give generously to private foundations that help fund that research. In this op-ed, I look at how these organizations fit into the national research landscape compared to funding by the NIH and I urge everyone to contact their representatives in Congress since even a small increase in the NIH budget can have a huge impact on research funding that is available to fight disease.


Author(s)
Ehtesham Arif

Address
Renal Electrolytes and Hypertension Division, UPenn, 3400 Civic Center Blvd, Philadelphia, PA 19104, USA
Abstract:

Availing the opportunity to get an independent research grant at the postdoctoral level not only provides encouragement and stability but also opens up new avenues of research and academic success. Awareness about research grants in terms of availability, eligibilities as well as a good research plan increases the chance of success. The present article is inspired by my research experiences in the United States. I tried to compile the sources for research grants, their eligibilities, and provide basic knowledge about how to design and write a proposal that will have the best chance for success. In my opinion this commentary will benefit the early stage researchers, especially non-immigrant researchers within the United States.


Author(s)
Stefanie B. Marquez
Address
UF, 2033 Mowry Road Cancer Genetics Research Complex Room 290 Gainesville, FL 32610, USA
Abstract:

If you have recently accepted a postdoctoral position and have begun working as a postdoc, or are planning to pursue a second postdoc, there are many opportunities to improve your skills both within and outside of academics and your specific field of study. The suggestions offered in this paper are not all-inclusive by any means, and are meant to serve as guidelines to show postdocs what they can do, not necessarily what they should do. This is my perspective as a third-year postdoctoral researcher in the medical sciences.

 
     
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