Affiliations: | 2013 | Basic Medical Sciences | Purdue University, West Lafayette, IN, United States |
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Bojun Chen is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2015 — 2019 |
Chen, Bojun |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Novel Proteins Regulating Function and Expression of Slo-2 Potassium Channels @ University of Connecticut Sch of Med/Dnt
? DESCRIPTION (provided by applicant): Slo2 channels are high-conductance potassium channels widely expressed in the mammalian nervous system. They play important roles in controlling neuronal excitability by allowing a large outward current through the cell membrane. Recent studies have established a strong link between mutations of human Slo2 channels and epileptic disorders. The expression and physiological function of a potassium channel in vivo generally depend on a variety of regulatory proteins. With respect to Slo2 channels, however, very little is known about the regulatory proteins. The nematode C. elegans has a single mammalian Slo2 channel homologue known as SLO-2, which is also widely expressed in the nervous system and plays important roles in regulating neuronal functions. This project is to take advantage of the exceptional power of C. elegans molecular genetics to identify proteins that are important to SLO-2 function in vivo. Through a genetic screen for mutants that suppressed a lethargic phenotype caused by expressing a hyperactive SLO-2 in worms, two proteins (RSE-1 and ADR-1) were identified as novel regulators of SLO-2. RSE-1 is a homologue of human heterogeneous nuclear ribonucleoprotein U (hnRNP U) whereas ADR-1 is a homologue of human adenosine deaminases acting on RNA (ADARs). Both hnRNP U and ADARs have been implicated in neurological diseases including epilepsy but the mechanisms are unclear. A combination of electrophysiological, molecular biological and genetic approaches will be used to achieve three specific objectives: (1) understanding how RSE-1 controls SLO-2 expression; (2) understanding how ADR-1 modulates SLO-2 function; and (3) identifying additional molecules important to SLO-2 regulation in vivo. The long-term goal is to use new knowledge from worms to uncover novel human Slo2 channel regulators, and to elucidate how they contribute to physiological functions or pathological roles of human Slo2 channels.
|
0.961 |
2021 |
Chen, Bojun |
R35Activity Code Description: To provide long term support to an experienced investigator with an outstanding record of research productivity. This support is intended to encourage investigators to embark on long-term projects of unusual potential. |
Novel Regulators of Slo2 Potassium Channels @ University of Connecticut Sch of Med/Dnt
Abstract The focus of research in my lab is to determine how physiological functions of Slo2 channels are regulated by other proteins. Slo2 channels are a family of large-conductance potassium channels existing in mammals as well as invertebrates. Human and mouse each have two such channels: Slo2.1/Slick and Slo2.2/Slack, whereas the nematode C. elegans has only one, SLO-2. These channels are widely expressed in the nervous system, and play important roles in shaping neuronal firing properties. Mutations of Slack in humans often cause epilepsies and intellectual disability. Although physiological functions of Slo2 channels are expected to be dependent on many other regulatory proteins, molecular identities and their mechanisms of action are only beginning to be recognized. In the past few years, we identified several proteins required for SLO-2 physiological functions in C. elegans, including two RNA/DNA binding proteins (HRPU-2 and a SAFB-like transcription modulator tentatively named SLTM-1), one RNA editing modulator (ADR-1), one protein tyrosine phosphatase (tentatively named PTP-5), and one pseudokinase (SCYL-1), which all have mammalian homologs. Our results suggest that HRPU-2 and SLTM-1 regulate SLO-2 function through controlling the expression of PTP-5, whereas ADR-1 regulates SLO-2 function through enhancing the expression of SCYL-1. We have demonstrated that SCYL-1 increases SLO-2 activity through direct interactions, and this regulation is conserved between mammalian SCYL1 and Slack. In the next five years, our major goals are to determine how PTP-5 regulates SLO-2 function and whether the regulatory mechanism is conserved with human Slo2 and a human PTP-5 homolog, to determine how HRPU-2 and SLTM-1 regulate PTP-5 expression, and to identify putative proteins required for ADR-1- dependent SCYL-1 expression using a forward genetics approach. We envision that results from the proposed studies will not only provide important new knowledge about the regulation of worm SLO-2, but also have the potential to reveal evolutionarily conserved mechanisms of Slo2 channel regulation.
|
0.961 |