One of your colleagues has obtained a sample of muscle phonghorytaseb that is known to be relatvely inactive She hasapproached you for advice on how to set up an appropriate anay. She has the following items avalable, not al of whichare appropriate for thi study. Help her out by selecting the items that she should une and what their purpose in they. and then eplain why each of the oer item wodnot be uset1. 100 MAMP2. 100 uM GTP1. 100 M ge4. 100 uM gose phesphateS. Branched gon4Unbranched gvoopen7.50 m HEPES buffer, p75a.50 m potansium phonghate bufter, piH75wite outa short elanation for each of the above items, and upload vour anwers by the due dane.

muscle phosphorylase also called glycogen phosphorylase.

Ore of vr coleap has ainedaample of mule phohoryethkown to be reutely inace Sehas proched you tor adice on how to set upan ropriate y. Se has the floing item alae, not aof whh wepprriate for thi stuty. Hep her ot by wlecting the tems that he hod ueand what the prposeinthe H andthen eplain why ech of the her item wonet beet 1. 100 MAMP 2. 100 M GTP 3. 100 e

Ore of vr coleap has ainedaample of mule phohoryethkown to be reutely inace Sehas proched you tor adice on how to set upan ropriate y. Se has the floing item alae, not aof whh wepprriate for thi stuty. Hep her ot by wlecting the tems that he hod ueand what the prposeinthe H andthen eplain why ech of the her item wonet beet 1. 100 MAMP 2. 100 M GTP 3. 100 e

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter8: Muscle Physiology

Section: Chapter Questions

Problem 2TAHL

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Similar questions

A research scientist is developing a new drug that blocks muscle cellreceptors that, when activated, stimulate a muscle contraction. In her firstexperiment, she used 250 mg of the new drug but saw no effect. In hersecond experiment, she increased the dosage to 750 mg. This dosagewas successful in blocking the muscle stimulation. Explain why increasingthe dosage would affect the outcome of the experiment.
please explain in detail in your own words Why we need derived position. Aims of Passive ROM exercisedoes it prevent atrophy of a muscle or not?
Why is the latent period longer during an isotonic twitch of a skeletalmuscle fiber than it is during an isometric twitch?a. Excitation–contraction coupling is slower during an isotonic twitch.b. Action potentials propagate more slowly when the fiber is shortening,so extra time is required to activate the entire fiber.c. In addition to the time for excitation-contraction coupling, it takesextra time for enough cross-bridges to attach to make the tension in themuscle fiber greater than the load.d. Fatigue sets in much more quickly during isotonic contractions, andwhen muscles are fatigued the cross-bridges move much more slowly.e. The latent period is longer because isotonic twitches only occur in slow(type I) muscle fibers.
Which of the following properties is not common to allthree muscle tissues?a. excitabilityb. the need for ATPc. at rest, uses shielding proteins to cover actinbindingsitesd. elasticity
NAME THE CHEMICAL TRANSMISSION AND THE NERVOUS SYSTEMBETWEEN A MOTOR NEURONE AND A SKELETAL MUSCLE. ANDEXPLAIN THE STEPS OF THIS CHEMICAL TRANSMISSION ONSKELETAL MUSCLES.
Antigarvity muscles maintain stretch reflex for prolonged periods withoutfatigue, because :-a- they are heavily innervated by α -motor neuronsb- they obtain their energy needs mainly from anaerobic metabolic processesc- they contain exceptionally high levels of creatine phosphated- they are rich in mitochondria
Fast-twitch muscle fibers have which of the following characteristics?a. fewer number of mitochondriab. rely on fermentation and creatine phosphate pathwaysc. are primarily anaerobicd. provide for a quick release of energye. All of these are correct.
Recently, it has been observed that several muscle diseases and disorders are linked to problems with triad structure and function.One such disorder is called malignant hyperthermia, a dire hypermetabolic response to certain inhaled anesthetics such as halothane. Muscles become very rigid due to excessive contraction (especially the masseter muscle), the body temperature spikes, andmuscles break down. Death is certain if not treated. Given the principal symptoms of malignant hyperthermia, what is its likely cause?Propose a theoretical mechanism for a treatment that would dampen the deleterious effects of this disorder.
How do calcium ionsparticipate in musclecontraction? Why do bothmuscle contraction andmuscle relaxation spendenergy?
The disease poliomyelitis (po′le-o-mi′˘e-li′tis) destroys motor neurons, causingloss of muscle function and even flaccid paralysis. Some patients recoverbecause axon branches form from the remaining motor neurons. Thesebranches innervate the paralyzed muscle fibers to produce motor unitswith many more muscle fibers than usual. How does this reinnervation ofmuscle fibers affect the degree of muscle control in a person who hasrecovered from poliomyelitis?
An antibody has been isolated that binds to F-actin but not to G-actin. Whatstructural feature(s) of F-actin do you suppose the antibody binds (i.e., howis the antibody able to distinguish between these two forms of actin)?
Every skeletal muscle fiber is supplied by a motor neuron at the NMJ. Watch this video (http://openstaxcollege.org/l/skelmuscfiber) to learn more about what happens at the neuromuscular junction. (a) What is the definition of a motor unit? (b) What is the structural and functional difference between a large motor unit and a small motor unit? Can you give an example of each? (c) Why is the neurotransmitter acetylcholine degraded after binding to its receptor?