Answer:
No
Explanation:
Fishes lay eggs and are not warm blooded vertebrates and don't have hair or fur
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Penicillins disrupts bacterial cell wall synthesis.
<h3>
How does penicillin affect bacterial cell walls?</h3>
- Penicillin kills bacteria by inhibiting the proteins which cross-link peptidoglycans in the cell wall .
- When a bacterium divides in the presence of penicillin, it cannot fill in the “holes” left in its cell wall.
- β-Lactam antibiotics, including penicillins, cephalosporins, monobactams, and carbapenems, are distinguished by a lactam ring in their molecular structure and act by inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls.
- Penicillins work by bursting the cell wall of bacteria. Drugs in the penicillin class work by indirectly bursting bacterial cell walls.
- They do this by acting directly on peptidoglycans, which play an essential structural role in bacterial cells.
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I think your right thats what i think it is two
Answer:
- Calcium binds to troponin C
- Troponin T moves tropomyosin and unblocks the binding sites
- Myosin heads join to the actin forming cross-bridges
- ATP turns into ADP and inorganic phosphate and releases energy
- The energy is used to impulse myofilaments slide producing a power stroke
- ADP is released and a new ATP joins the myosin heads and breaks the bindings to the actin filament
- ATP splits into ADP and phosphate, and the energy produced is accumulated in the myosin heads, starting a new cycle
- Z-bands are pulled toward each other, shortening the sarcomere and the I-band, producing muscle fiber contraction.
Explanation:
In rest, the tropomyosin inhibits the attraction strengths between myosin and actin filaments. Contraction initiates when an action potential depolarizes the inner portion of the muscle fiber. Calcium channels activate in the T tubules membrane, releasing <u>calcium into the sarcolemma.</u> At this point, tropomyosin is obstructing binding sites for myosin on the thin filament. When calcium binds to troponin C, troponin T alters the tropomyosin position by moving it and unblocking the binding sites. Myosin heads join to the uncovered actin-binding points forming cross-bridges, and while doing so, ATP turns into ADP and inorganic phosphate, which is released. Myofilaments slide impulsed by chemical energy collected in myosin heads, producing a power stroke. The power stroke initiates when the myosin cross-bridge binds to actin. As they slide, ADP molecules are released. A new ATP links to myosin heads and breaks the bindings to the actin filament. Then ATP splits into ADP and phosphate, and the energy produced is accumulated in the myosin heads, which starts a new binding cycle to actin. Finally, Z-bands are pulled toward each other, shortening the sarcomere and the I-band, producing muscle fiber contraction.