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Articles 1 - 5 of 5

Full-Text Articles in Biochemistry, Biophysics, and Structural Biology

Hyper-Activation Of Pp60(Src) Limits Nitric Oxide Signaling By Increasing Asymmetric Dimethylarginine Levels During Acute Lung Injury, Sanjiv Kumar, Xutong Sun, Satish Kumar Noonepalle, Qing Lu, Evgeny Zemskov, Ting Wang, Saurabh Aggarwal, Christine Gross, Shruti Sharma, Ankit A. Sesai, John D. Catravas Jan 2017

Hyper-Activation Of Pp60(Src) Limits Nitric Oxide Signaling By Increasing Asymmetric Dimethylarginine Levels During Acute Lung Injury, Sanjiv Kumar, Xutong Sun, Satish Kumar Noonepalle, Qing Lu, Evgeny Zemskov, Ting Wang, Saurabh Aggarwal, Christine Gross, Shruti Sharma, Ankit A. Sesai, John D. Catravas

Bioelectrics Publications

The molecular mechanisms by which the endothelial barrier becomes compromised during lipopolysaccharide (LPS) mediated acute lung injury (ALI) are still unresolved. We have previously reported that the disruption of the endothelial barrier is due, at least in part, to the uncoupling of endothelial nitric oxide synthase (eNOS) and increased peroxynitrite-mediated nitration of RhoA. The purpose of this study was to elucidate the molecular mechanisms by which LPS induces eNOS uncoupling during ALI. Exposure of pulmonary endothelial cells (PAEC) to LPS increased pp60Src activity and this correlated with an increase in nitric oxide (NO) production, but also an increase in ...


Excitatory Transmission Onto Agrp Neurons Is Regulated By Cjun Nh2-Terminal Kinase 3 In Response To Metabolic Stress, Santiago Vernia, Caroline Morel, Joseph C. Madara, Julie Cavanagh-Kyros, Tamera Barrett, Kathryn O. Chase, Norman J. Kennedy, Dae Young Jung, Jason K. Kim, Neil Aronin, Richard A. Flavell, Bradford B. Lowell, Roger J. Davis Feb 2016

Excitatory Transmission Onto Agrp Neurons Is Regulated By Cjun Nh2-Terminal Kinase 3 In Response To Metabolic Stress, Santiago Vernia, Caroline Morel, Joseph C. Madara, Julie Cavanagh-Kyros, Tamera Barrett, Kathryn O. Chase, Norman J. Kennedy, Dae Young Jung, Jason K. Kim, Neil Aronin, Richard A. Flavell, Bradford B. Lowell, Roger J. Davis

Davis Lab Publications

The cJun NH2-terminal kinase (JNK) signaling pathway is implicated in the response to metabolic stress. Indeed, it is established that the ubiquitously expressed JNK1 and JNK2 isoforms regulate energy expenditure and insulin resistance. However, the role of the neuron-specific isoform JNK3 is unclear. Here we demonstrate that JNK3 deficiency causes hyperphagia selectively in high fat diet (HFD)-fed mice. JNK3 deficiency in neurons that express the leptin receptor LEPRb was sufficient to cause HFD-dependent hyperphagia. Studies of sub-groups of leptin-responsive neurons demonstrated that JNK3 deficiency in AgRP neurons, but not POMC neurons, was sufficient to cause the hyperphagic response. These ...


Nuclear Localization Of Cpi-17, A Protein Phosphatase-1 Inhibitor Protein, Affects Histone H3 Phosphorylation And Corresponds To Proliferation Of Cancer And Smooth Muscle Cells., Masumi Eto, Jason A Kirkbride, Rishika Chugh, Nana Kofi Karikari, Jee In Kim Apr 2013

Nuclear Localization Of Cpi-17, A Protein Phosphatase-1 Inhibitor Protein, Affects Histone H3 Phosphorylation And Corresponds To Proliferation Of Cancer And Smooth Muscle Cells., Masumi Eto, Jason A Kirkbride, Rishika Chugh, Nana Kofi Karikari, Jee In Kim

Department of Molecular Physiology and Biophysics Faculty Papers

CPI-17 (C-kinase-activated protein phosphatase-1 (PP1) inhibitor, 17kDa) is a cytoplasmic protein predominantly expressed in mature smooth muscle (SM) that regulates the myosin-associated PP1 holoenzyme (MLCP). Here, we show CPI-17 expression in proliferating cells, such as pancreatic cancer and hyperplastic SM cells. Immunofluorescence showed that CPI-17 was concentrated in nuclei of human pancreatic cancer (Panc1) cells. Nuclear accumulation of CPI-17 was also detected in the proliferating vascular SM cell culture and cells at neointima of rat vascular injury model. The N-terminal 21-residue tail domain of CPI-17 was necessary for the nuclear localization. Phospho-mimetic Asp-substitution of CPI-17 at Ser12 attenuated the nuclear ...


Requirement Of Jip Scaffold Proteins For Nmda-Mediated Signal Transduction, Norman J. Kennedy, Gilles Martin, Anka G. Ehrhardt, Julie Cavanagh-Kyros, Chia-Yi Kuan, Pasko Rakic, Richard A. Flavell, Steven N. Treistman, Roger J. Davis Sep 2007

Requirement Of Jip Scaffold Proteins For Nmda-Mediated Signal Transduction, Norman J. Kennedy, Gilles Martin, Anka G. Ehrhardt, Julie Cavanagh-Kyros, Chia-Yi Kuan, Pasko Rakic, Richard A. Flavell, Steven N. Treistman, Roger J. Davis

Davis Lab Publications

JIP scaffold proteins are implicated in the regulation of protein kinase signal transduction pathways. To test the physiological role of these scaffold proteins, we examined the phenotype of compound mutant mice that lack expression of JIP proteins. These mice were found to exhibit severe defects in N-methyl-D-aspartic acid (NMDA) receptor function, including decreased NMDA-evoked current amplitude, cytoplasmic Ca(++), and gene expression. The decreased NMDA receptor activity in JIP-deficient neurons is associated with reduced tyrosine phosphorylation of NR2 subunits of the NMDA receptor. JIP complexes interact with the SH2 domain of cFyn and may therefore promote tyrosine phosphorylation and activity of ...


The Second Messenger Camp Elicits Eating By An Anatomically Specific Action In The Perifornical Hypothalamus, Elizabeth R. Gillard, Arshad M. Khan, Rickinder S. Grewal, Bara Mouradi, Stefany D. Wolfsohn, B. Glenn Stanley Mar 1998

The Second Messenger Camp Elicits Eating By An Anatomically Specific Action In The Perifornical Hypothalamus, Elizabeth R. Gillard, Arshad M. Khan, Rickinder S. Grewal, Bara Mouradi, Stefany D. Wolfsohn, B. Glenn Stanley

Arshad M. Khan, Ph.D.

No abstract provided.