A new drug (Compound Y) is developed for treatment of cancer. Initial studies on isolated cells show that Compound Y decreases cancer cell viability by 95%. However, when Compound Y is tested on ventricular cardiac myocytes it is observed that it causes a significant reduction in delayed rectifier K+ channel current. Why could Compound Y NOT be taken forward to clinical trials?

A new drug (Compound Y) is developed for treatment of cancer. Initial studies on isolated cells show that Compound Y decreases cancer cell viability by 95%. However, when Compound Y is tested on ventricular cardiac myocytes it is observed that it causes a significant reduction in delayed rectifier K+ channel current. Why could Compound Y NOT be taken forward to clinical trials?

Biomedical Instrumentation Systems

1st Edition

ISBN:9781133478294

Author:Chatterjee

Publisher:Chatterjee

Chapter13: Artifacts And Noise In Medical Instrumentation

Section: Chapter Questions

Problem 1CS

See similar textbooks

Similar questions

Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions How would you determine robustness of the assay and validate the assay?
Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions How would you apply a TR-FRET assay to measure the in vitro kinase activity of VEGFR-2? Describe in steps the assay design and potential readout outcome.
Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions What is the advantage of measuring autophosphorylation of the receptor rather than phosphorylation of the substrate?
Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions While setting up your experiment, you accidentally discovered autophophorylation of receptor. What observation/results led you to believe that there was autophosphorylation of the receptor?
when calculating the Resting membrance potential using the goldman equation it is usally out, out , in / in, in, out. the cl- is switched so does that mean that when writing the in and out cellular concentartion should we still add negative sign in front of the value or since it is flipped we shouldnt?.
The typical distribution of K+ and Na+ ions inside and outside the cell is: [K+]in = 150 mM; [K+]out = 5 mM; [Na+]in = 10 mM; [Na+]out = 150 mM What are reversal potentials for Na+ and K+ at 25oC ? What should be the ratios of PNa/PK at (i) rest (-60 mV) and (ii) during the action potential (+20 mV) to generate a spike from -60 to +20 mV. Use the short form of Goldman equation.
It is not an easy matter to assign particular func-tions to specific components of the basal lamina, sincethe overall structure is a complicated composite materialwith both mechanical and signaling properties. Nidogen,for example, cross-links two central components of thebasal lamina by binding to the laminin γ-1 chain and totype IV collagen. Given such a key role, it was surprisingthat mice with a homozygous knockout of the gene fornidogen-1 were entirely healthy, with no abnormal phe-notype. Similarly, mice homozygous for a knockout of thegene for nidogen-2 also appeared completely normal. Bycontrast, mice that were homozygous for a defined muta-tion in the gene for laminin γ-1, which eliminated just thebinding site for nidogen, died at birth with severe defectsin lung and kidney formation. The mutant portion of thelaminin γ-1 chain is thought to have no other functionthan to bind nidogen, and does not affect laminin struc-ture or its ability to assemble into the basal lamina.…
Nodal (conductile) cells in the heart differ from other myocardiocytes (contractile cells) in that nodal cells have_____. A channels that allow Na+ to slowly leak in between action potentials B gap junctions while other myocardiocytes do not C more rapid depolarization in their action potentials due to voltage-gated Na+ channels D action potentials without plateau phases because they lack Ca+2 channels
Describe why a doctor would give a patient that is diagnosed with acute myocardial infarction the treatment of tissue plasminogen activator(tPA)? What will it do?
Two GPCR mutations (Mutant A and Mutant B) were tested for activity. One was confirmed as being a constitutively activating, gain of function GPCR mutation and one was confirmed as being a loss of function GPCR mutation. Which is which? Explain your answer.
Which statement does not apply to macroscopic whole cell currents? Group of answer choices -Can be recorded using the patch clamp technique in the whole cell configuration. -All of these statements apply to macroscopic whole cell currents. -Are the sum current of single channel currents (i.e. through hundreds to thousands of ion channels). -Can be recorded using both inside-out and outside-out patch configurations. -Reflect population-level activation and inactivation properties of ion channels.
What features of the bypass polymerase make it ideal forits role in translesion synthesis, shown in Figure 16-24?