Open Access. Powered by Scholars. Published by Universities.®
- Keyword
- Publication Year
Articles 1 - 21 of 21
Full-Text Articles in Life Sciences
Beneficial Aerodynamic Effect Of Wing Scales On The Climbing Flight Of Butterflies, Nathan Slegers, Michael Heilman, Jacob Cranford, Amy Lang, John Yoder, Maria Laura Habegger
Beneficial Aerodynamic Effect Of Wing Scales On The Climbing Flight Of Butterflies, Nathan Slegers, Michael Heilman, Jacob Cranford, Amy Lang, John Yoder, Maria Laura Habegger
Faculty Publications - Biomedical, Mechanical, and Civil Engineering
It is hypothesized that butterfly wing scale geometry and surface patterning may function to improve aerodynamic efficiency. In order to investigate this hypothesis, a method to measure butterfly flapping kinematics optically over long uninhibited flapping sequences was developed. Statistical results for the climbing flight flapping kinematics of 11 butterflies, based on a total of 236 individual flights, both with and without their wing scales, are presented. Results show, that for each of the 11 butterflies, the mean climbing efficiency decreased after scales were removed. Data was reduced to a single set of differences of climbing efficiency using are paired t …
Identification And Rna Binding Characterization Of Plant Virus Rna Silencing Suppressor Proteins, Jeff Vargason, Carissa J. Burch, Jesse W. Wilson
Identification And Rna Binding Characterization Of Plant Virus Rna Silencing Suppressor Proteins, Jeff Vargason, Carissa J. Burch, Jesse W. Wilson
Faculty Publications - Department of Biological & Molecular Science
Suppression is a common mechanism employed by viruses to evade the antiviral effects of the host’s RNA silencing pathway. The activity of suppression has commonly been localized to gene products in the virus, but the variety of mechanisms used in suppression by these viral proteins spans nearly the complete biochemical pathway of RNA silencing in the host. This review describes the agrofiltration assay and a slightly modified version of the agro-infiltration assay called co-infiltration, which are common methods used to observe RNA silencing and identify viral silencing suppressor proteins in plants, respectively. In addition, this review will provide an overview …
Akap7 Regulates Cam Kinase Activation In Mcf-7 Cells, John M. Schmitt, Hannah M. Mcfarland, Kimberly Dodge-Kafka
Akap7 Regulates Cam Kinase Activation In Mcf-7 Cells, John M. Schmitt, Hannah M. Mcfarland, Kimberly Dodge-Kafka
Faculty Publications - Department of Biological & Molecular Science
Abstract Estrogen (E2) activates calcium/calmodulin-dependent protein kinases (CaM Kinases) in MCF-7 breast cancer cells. In particular E2 activates a CaM KK, CaM KI, and ERK pathway to promote proliferation. CaM Kinase activation of ERK may be blocked by PKA in certain cell types through direct phosphorylation and inhibition of CaM KK. The ability of PKA to phosphorylate its cellular targets may be dictated by protein kinase A anchoring proteins (AKAPs). Hormones that elevate cAMP and activate PKA may utilize AKAPs to regulate signal transduction. Our goal was to evaluate the role of AKAPs in regulating E2 activation of the CaM …
Estrogen Receptor Α Regulates Erk In Mcf-7 Cells, John M. Schmitt, Angela J. Rofelty
Estrogen Receptor Α Regulates Erk In Mcf-7 Cells, John M. Schmitt, Angela J. Rofelty
Faculty Publications - Department of Biological & Molecular Science
Abstract Estrogen (E2) signaling significantly affects breast tumorigenesis by enhancing cell growth and preventing apoptosis. The actions of estrogen in MCF-7 breast cancer cells are mediated through a kinase pathway involving CaM KK, CaM KI, and ERK. Current research is examining the involvement of the Estrogen Receptor (ER) alpha (α) and beta (β) as well as G-Protein Coupled Receptor GPR30 in cell growth and proliferation. ERα is suggested to be responsible for ERK and perhaps CaM Kinase activation. Our goal was to evaluate if ERα, rather than GPR30 or ERβ, mediates CaM KI and ERK activation upon treatment of MCF-7 …
Cam Kk Mediates Mdm2 Activation In Lncap Cells, John M. Schmitt, Philip Graber
Cam Kk Mediates Mdm2 Activation In Lncap Cells, John M. Schmitt, Philip Graber
Faculty Publications - Department of Biological & Molecular Science
Abstract Agonists and hormones that cause an influx of calcium in LNCaP prostate cancer cells activate the calcium/calmodulin-dependent protein kinase (CaM Kinase) pathway and AKT phosphorylation. CaM KK and AKT are essential for promoting LNCaP cell survival. AKT phosphorylation of MDM2 protein may negatively regulate the tumor suppressor protein, p53. CaM KK and AKT have yet to be demonstrated as upstream regulators of MDM2 and p53 in LNCaP cells. Our goals were to examine the ability of carbachol and testosterone to stimulate MDM2 phosphorylation, its association with p53, and whether CaM KK is upstream of MDM2. Stimulation of LNCaP cells …
Estrogen Regulation Of Jun And Fos In Mcf-7 Cells, John M. Schmitt, Renee Geck, Jessica N. Magill
Estrogen Regulation Of Jun And Fos In Mcf-7 Cells, John M. Schmitt, Renee Geck, Jessica N. Magill
Faculty Publications - Department of Biological & Molecular Science
Abstract C-Fos and c-Jun are transcription factors that form the dimer Activator Protein 1 (AP-1) and bind DNA to initiate transcription. C-Fos, c-Jun are targets of the Extracellular Signal-Regulated Kinase (ERK) in multiple cell types, including MCF-7 breast cancer cells. The hormone estrogen (E2) can increase intracellular calcium levels which activates calcium/calmodulin-dependent kinase (CaM Kinase) proteins, which control ERK and gene transcription. Our goal was to evaluate the ability of E2 to activate c-Fos and c-Jun and induce their dimerization, via CaM KK and ERK, in MCF-7 cells. Interestingly, E2 stimulation of MCF-7 cells triggered phosphorylation of c-Jun and c-Fos …
Estrogen And Vitamin D Control Of Transcription In Mcf-7 Cells, John M. Schmitt, N. Magill
Estrogen And Vitamin D Control Of Transcription In Mcf-7 Cells, John M. Schmitt, N. Magill
Faculty Publications - Department of Biological & Molecular Science
Abstract The Extracellular Signal-Regulated Kinase (ERK) is part of a key, signaling pathway that regulates both transcription and translation in many cell types. Increases in intracellular calcium levels results in the CaM Kinase-dependent activation of ERK and cell growth in MCF-7 breast cancer cells. ERK has also been shown to play a role in the regulation of MCF-7 cell proliferation through control of downstream transcription factors including Elk-1. The hormone, Vitamin D has been suggested to play an inhibitory role on cancer cells by blocking ERK activation. Our goal was to evaluate the ability of E2 to activate Elk-1, through …
Estrogen Receptor Activation Of Cam Kinase I And Erk, John M. Schmitt, Mikayla S. Todd
Estrogen Receptor Activation Of Cam Kinase I And Erk, John M. Schmitt, Mikayla S. Todd
Faculty Publications - Department of Biological & Molecular Science
Cell growth and development is regulated by the cell signaling second messenger, calcium, that regulates key enzymes and genes in cells including the Calcium/Calmodulin-dependent protein kinases (CaM Ks) and their downstream target ERK. In particular, CaM KK and its substrate CaM KI promote ERK and Elk-1 activation in MCF-7 breast cancer cells. Estrogen (E2) may utilize CaM KK and ERK to promote breast cancer cell proliferation, however it is unclear which E2 receptor promotes cell proliferation through CaM Ks. Estrogen is a ligand for estrogen receptors (ER) of the alpha(α) and beta(β) forms, as well as G protein-coupled receptor 30 …
Cam Kinase Regulation Of Akt And Bad In Prostate Cancer Cells, John M. Schmitt, Samantha F. Smith
Cam Kinase Regulation Of Akt And Bad In Prostate Cancer Cells, John M. Schmitt, Samantha F. Smith
Faculty Publications - Department of Biological & Molecular Science
Abstract AKT and its substrate BAD promote prostate cancer cell survival. Agonists, such as carbachol, and hormones that increase intracellular calcium concentration can activate AKT leading to cancer cell survival. LNCaP prostate cancer cells express the carbachol-sensitive M3-subtype of GPCR’s that increase intracellular calcium and activate the family of Ca2+/Calmodulin-dependent Protein Kinases (CaM Ks). One type of CaM Kinase, CaM Kinase Kinase (CaM KK), directly phosphorylates AKT on threonine 308. AKT phosphorylation and activation can enhance cell survival through phosphorylation BAD protein and the subsequent blockade of caspase activation. Our goals were to examine the mechanism of carbachol activation of …
14-3-3Γ Binds To Cam Kkα And Blocks Estrogen Signaling In Mcf-7 Cells, John M. Schmitt, Amanda P. Ankeny
14-3-3Γ Binds To Cam Kkα And Blocks Estrogen Signaling In Mcf-7 Cells, John M. Schmitt, Amanda P. Ankeny
Faculty Publications - Department of Biological & Molecular Science
Abstract Extracellular Signal-Regulated Kinase (ERK) is activated by estrogen (E2) downstream of CaM KK leading to cell growth in MCF-7 breast cancer cells. Previous studies have shown that ERK activation may be inhibited by cAMP and PKA. PKA has numerous cellular targets including CREB, Src, Raf-1, arrestins, and CaM KK. CaM KK is inhibited by direct PKA phosphorylation and the subsequent interaction with 14-3-3γ . Agonists that activate cAMP and PKA may block CaM KK activation of ERK and cell proliferation. Our goal was to evaluate the ability of cAMP and PKA to antagonize the effects of E2 on MCF-7 …
Transcription Factor Regulation Of Erk And Estrogen In Mcf-7 Cells, John M. Schmitt, Jessica N. Magill
Transcription Factor Regulation Of Erk And Estrogen In Mcf-7 Cells, John M. Schmitt, Jessica N. Magill
Faculty Publications - Department of Biological & Molecular Science
Abstract ERK is activated by increased intracellular calcium downstream of the hormone estrogen (E2). E2 activates ERK via the CaM Kinases, specifically CaM KK and CaM KI in MCF-7 cells. ERK may control cell growth and proliferation through Elk-1, Rsk, SRF, CREB, and numerous other molecules and nuclear targets. Vitamin D, a hormone, has proven to be an effective antagonist of ERK and MCF-7 breast cancer cell growth. Our goal was to evaluate if the E2 pathway working through CaM KK and ERK regulated the transcription factors Elk-1, CREB, and SRF. We also examined the ability of vitamin D to …
Trp Channel Regulation Of Estrogen Signaling, John M. Schmitt, Jessica N. Magill
Trp Channel Regulation Of Estrogen Signaling, John M. Schmitt, Jessica N. Magill
Faculty Publications - Department of Biological & Molecular Science
Abstract Calcium regulates numerous cell functions including growth and development. Calcium can enter cells through transient receptor potential channels (TRPCs). Previous studies in MCF-7 cells have suggested that the expression of one particular TRPC, TRPC6, correlates with cell transformation and disease progression. Calcium has several cellular targets including the Calcium/Calmodulin-dependent protein kinases (CaM Ks) and ERK. Previous work has shown that estrogen (E2) may utilize CaM Ks and ERK to promote breast cancer cell proliferation, however the possible involvement of TRPCs in this pathway is currently unknown. Our objective was to understand which E2 receptor is used in our system …
Erk Activation Requires Cam Kinases In Mcf-7 Breast Cancer Cells, John M. Schmitt, Ellen Abell
Erk Activation Requires Cam Kinases In Mcf-7 Breast Cancer Cells, John M. Schmitt, Ellen Abell
Faculty Publications - Department of Biological & Molecular Science
Abstract A key signaling pathway involved in regulating cell growth and proliferation throughout the body is the ERK signaling pathway. ERK is activated via numerous pathways including intracellular calcium release downstream of G-Protein Coupled Receptors (GPCRs). Carbachol, a GPCR-agonist, both increases intracellular calcium and ERK activation in MCF-7 cells. ERK activation and control of cell growth may act through the transcription factor Elk-1. Our goal was to elucidate the specific proteins and kinases upstream of ERK in MCF-7 cells treated with carbachol. Secondly, we wanted to investigate the potential involvement of Elk-1 downstream of ERK. Carbachol treatment of MCF-7 cells …
Cam Kinase Kinase Control Of Prostate Cancer Cell Survival, John M. Schmitt, Brendon Hart
Cam Kinase Kinase Control Of Prostate Cancer Cell Survival, John M. Schmitt, Brendon Hart
Faculty Publications - Department of Biological & Molecular Science
Abstract AKT has been implicated in promoting cell survival within certain cells. Current research has shown that hormones that increase the concentration of intracellular calcium can activate AKT that in turn leads to cancer cell survival. Interestingly, LNCaP cells express the M3-subtype of GPCR's that may couple to increases in intracellular calcium and activation of the Ca2+/Calmodulin-dependent Protein Kinases (CaM Ks). Specifically CaM Kinase Kinase (CaM KK) phosphorylates its direct substrates CaM Kinase I, CaM Kinase IV, and AKT. AKT promotes cell survival through phosphorylation of its target BAD that prevents caspase activation. Our goals were to examine the mechanism …
M3-Muscarinic Receptor Activation Of Erk And Cell Growth Requires Calcium/Calmodulin-Dependent Protein Kinases In Mcf-7 Cells, John M. Schmitt, Ellen Abell, Andrea Wagner
M3-Muscarinic Receptor Activation Of Erk And Cell Growth Requires Calcium/Calmodulin-Dependent Protein Kinases In Mcf-7 Cells, John M. Schmitt, Ellen Abell, Andrea Wagner
Faculty Publications - Department of Biological & Molecular Science
Abstract The extracellular signal-regulated protein kinase (ERK) signaling pathway is found in diverse cells throughout the human body. ERK activation has been implicated in breast cancer cell growth and proliferation. Studies have shown that ERK is activated by carbachol, a G Protein-Coupled Receptor (GPCR) agonist, which increases intracellular calcium in MCF-7 cells. The calcium/calmodulin-dependent protein kinase (CaM K) family of proteins including CaM KK, CaM KI, and CaM KII can be activated by increased intracellular calcium. Our goal was to determine whether CaM Ks may be responsible for ERK activation and cell proliferation in carbachol-treated MCF-7 cells and evaluate which …
Carbachol Regulation Of Akt In Lncap Prostate Cancer Cells, John M. Schmitt, Luke Fletcher
Carbachol Regulation Of Akt In Lncap Prostate Cancer Cells, John M. Schmitt, Luke Fletcher
Faculty Publications - Department of Biological & Molecular Science
Abstract Hormones and agonists that enhance cell survival through binding specific G Protein-Coupled Receptors (GPCRs) are of particular interest in cancer cell survival. LNCaP cells have been shown to express muscarinic cholinergic receptors that are responsive to the agonist, carbachol. In addition, LNCaP cells specifically express the M3-subtype of GPCR’s that may couple carbachol to Gq, increases in intracellular calcium, and activation of the intracelluar Ca2+/calmodulin-dependent protein kinases (CaM Ks). The CaM Kinase family of proteins includes CaM KII, CaM Kinase Kinase (CaM KK) and its substrates CaM KIV, CaM KI and the protein kinase AKT. AKT is an anti-apoptotic …
“Carbachol Regulation Of Erk And The Transcription Factor Elk-1 In Mcf-7 Breast Cancer Cells, John M. Schmitt, Andrea Wagner
“Carbachol Regulation Of Erk And The Transcription Factor Elk-1 In Mcf-7 Breast Cancer Cells, John M. Schmitt, Andrea Wagner
Faculty Publications - Department of Biological & Molecular Science
Abstract Cancer has numerous molecular, biochemical and physiological hallmarks including uncontrolled cell growth and proliferation. Previous studies on MCF-7 breast cancer cells have shown that both intracellular calcium levels and the extracellular signal-regulated protein kinase (ERK) is activated downstream of the G-protein coupled receptor (GPCR) agonist, carbachol. Calcium/calmodulin regulate the calcium/calmodulin-dependent kinase (CaM Ks) family of proteins that have been proposed to regulate ERK and transcription. Our goal was to determine the mechanism of carbachol activation on ERK and the transcription factor Elk-1 in MCF-7 cells. Our results suggest that 10 μM carbachol treatment of MCF-7 cells triggers ERK1/2 phosphorylation …
Distributions Of Z-Dna And Nuclear Factor I In Human Chromosome 22: A Model For Coupled Transcriptional Regulation, P. Christoph Champ, Sandor Maurice, Jeff Vargason, Tracy Camp, P. Shing Ho
Distributions Of Z-Dna And Nuclear Factor I In Human Chromosome 22: A Model For Coupled Transcriptional Regulation, P. Christoph Champ, Sandor Maurice, Jeff Vargason, Tracy Camp, P. Shing Ho
Faculty Publications - Department of Biological & Molecular Science
An analysis of the human chromosome 22 genomic sequence shows that both Z-DNA forming regions (ZDRs) and promoter sites for nuclear factor-I (NFI) are correlated with the locations of known and predicted genes across the chromosome and accumulate around the transcriptional start sites of the known genes. Thus, the occurrence of Z-DNA across human genomic sequences mirrors that of a known eukaryotic transcription factor. In addition, 43 of the 383 fully annotated chromosomal genes have ZDRs within 2 nucleosomes upstream of strong NFIs. This suggests a distinct class of human genes that may potentially be transcriptionally regulated by a mechanism …
The Effect Of Cytosine Methylation On The Structure And Geometry Of The Holliday Junction: The Structure Of D(Ccggtacm5 Cgg) At 1.5 Å Resolution, Jeff Vargason, P. Shing Ho
The Effect Of Cytosine Methylation On The Structure And Geometry Of The Holliday Junction: The Structure Of D(Ccggtacm5 Cgg) At 1.5 Å Resolution, Jeff Vargason, P. Shing Ho
Faculty Publications - Department of Biological & Molecular Science
No abstract provided.
A Crystallographic Map Of The Transition From B-Dna To A-Dna, Jeff Vargason, Keith Henderson, P. Shing Ho
A Crystallographic Map Of The Transition From B-Dna To A-Dna, Jeff Vargason, Keith Henderson, P. Shing Ho
Faculty Publications - Department of Biological & Molecular Science
No abstract provided.
The Holliday Junction In An Inverted Repeat Dna Sequence: Sequence Effects On The Structure Of Four-Way Junctions, Brandt F. Eichman, Jeff Vargason, Blaine H.M. Mooers, P. Shing Ho
The Holliday Junction In An Inverted Repeat Dna Sequence: Sequence Effects On The Structure Of Four-Way Junctions, Brandt F. Eichman, Jeff Vargason, Blaine H.M. Mooers, P. Shing Ho
Faculty Publications - Department of Biological & Molecular Science
Holliday junctions are important structural intermediates in recombination, viral integration, and DNA repair. We present here the single-crystal structure of the inverted repeat sequence d(CCGGTACCGG) as a Holliday junction at the nominal resolution of 2.1 Å. Unlike the previous crystal structures, this DNA junction has B-DNA arms with all standard Watson–Crick base pairs; it therefore represents the intermediate proposed by Holliday as being involved in homologous recombination. The junction is in the stacked-X conformation, with two interconnected duplexes formed by coaxially stacked arms, and is crossed at an angle of 41.4° as a right-handed X. A sequence comparison with previous …