Syt1 point mutation is a point mutation in synaptotagmin-1. A. How did the experiment shown in the figure below show that synaptotagmin was probably the Ca²+ sensor? of synaptic response 1.5 1.0 50.5 Syt1 point mutation wild type (MM) 10
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Synaptotagmin-1, a protein that detects calcium ions at synapses, collaborates with the SNARE complex, a collection of proteins, to aid in the fusion of vesicles with cell membranes. Three distinct structures of synaptotagmin-1 coupled to the SNARE complex have been described in earlier research. Which of these binding states, though, truly causes the release of neurotransmitters was unclear.
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- From experiments in which cells expressing normal myosin II heavy chain were altered to either lack (mhckA-) or overexpress (MHCKA ++) a myosin heavy chain kinase (MHCKA). For answering this question recall the earlier the variants on the myosin II heavy chain, in which three key threonines, normally subject to reversible phosphorylation, were altered in various ways: 3X Ser = Serines in place of Threonines 3X Ala = Alanines in place of Threonines 3X Asp = Aspartate in place of Threonines MHCKA is present at normal levels. Which of the two mutants (mhcp- or MHCP++) would be most likely to have a defect in cytokinesis?Many enzymes can hydrolyze GTP between the β and γ phosphates. The GTP analog β,γ-imidoguanosine 5′-triphosphate (Gpp(NH)p), shown below, cannot be hydrolyzed between the β and γ phosphates. Predict the effect of microinjection of Gpp(NH)p into a myocyte on the cell’s response to β-adrenergic stimulation.Which of the following would you expect to happen if amino acids 579 to 582 (YIYV) in the PDGF-Beta receptor were exchanged with amino acids 992 to 995 (YLIP) from the EGF receptor to give PDGF (YLIP) and EGF (YIYV) (Select all that apply)? (A) PDGF-B receptor Src I NCK-B SHP2 PLC-y P 579 P 581 YIYV PI3KY P 740 YMDM NCK-a P 751 YVPM P 771 YMAP GAP P 1009 YTAV P 1021 YIIP (B) POE 845 YHAE 992 YLIP 1045 YSSD 1068 YINQ 1086 YHNK 1148 YQQD 1173 YLRV P P P P P P P EGF receptor STAT3/5 PLC-y Shc Cbl JAK2 Grb2 STAT3/5 Shc SHP1 PTP1
- 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.In Chapter 3, the Kd of calmodulin EF hands for binding Ca2+ is given as 10−6 M. Many proteins have much higher affinities for their respective ligands. Why is the specific affinity of calmodulin important for Ca2+ signaling pro- cesses such as that initiated by production of IP3?2022) . Join: 739526. P 7 R 888 F4 Chemical messengers that cross the synapse bind to _ channels, which create. Select an answer and submit. For keyboard navigation, use the up/down arrow keys to select an answer. b a Ligand gated; Action с ce7-4f96-ba96-ba1e2373d5e9 Wk7: Q5 Homework Unanswered Due Today, 11:59 PM d Voltage gated; Graded Ligand gated; Graded Voltage gated; Action Unanswered. 2 attempts left % 5 OCT 19 F5 T ^ 6 ♫ dity STA e MacBook Air F6 Y & 7 F7 C * 00 8 DII FB ( 9 potentials. DD F9 O ) O F10 P F11 No C Subm + =
- alpha 1 adrenergic receptor causes vasoconstriction through activation of Gq protein explain the mechanism of action for this receptorb starting from the ligand binding step untill final effectoe is activatedWhich ONE of these statements is the most accurate definition of the mode of action of imatinib? Select one: A.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by competing with adenosine triphosphate (ATP) binding B.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by competing with adenosine triphosphate (ATP) binding C.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by interaction with the enzyme site D.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by interaction with the enzyme site2+ Activation of 5-HT2A Increases cytosolic free Ca²+ Concentration ([Ca²+]) Via a Signaling cascade. At rest, neurons have a cytosolic Ca Concentration of 100nM. The ex- Tra cellular free calcium concentration is typically 1.2m M. Calculate the resting potential (at equilibrium) produced by the neuron as a result of the calcium ion concentration gradient. (Report your answer in mV ).
- 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.added ligand concentration of 10 µM is 5 × 10³ s¹. What is the value of the reverse rate constant k_1 = 1 ×10-4 Incorrect Macmillan Learning You have not correctly calculated the value of the reverse rate constant. To begin, calculate the value of k₁ by dividing the rate of receptor-ligand complex formation (the rate of the forward reaction) by the ligand concentration. k₁ = rate forward [L] Then, calculate the value of the reverse rate constant, k_₁, by multiplying the dissociation constant, Kd, and the forward rate constant, k₁. k_1 = Kak₁The top panel (a) of this figure shows the graded potential change (far right, upper, electrical trace) that results from ligand binding to the ligand gated Na+ channel. The bottom panel of this figure (b) shows a graded potential change (far right, lower, electrical trace) that results from ligand binding to a ligand gated Cl- channel. From this trace you know (Vm = -70 mV) 1. ECl- is -70 mV 2. ECl- is more negative than -70 mV (i.e., -80 mV) 3. ECl- is more positive than -70 mV (i.e., -60 mV)