CPN60 is not involved in Heat Shock response.

A. Workflow of HS experiments and representative blood smears. Parasites are subjected to HS at 40oC for 24 hours and then allowed to recover at normal temperature (37oC). B. Parasites were subjected to HS and recovery as depicted in (A). Left:...

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Λεπτομέρειες βιβλιογραφικής εγγραφής
Κύριος συγγραφέας:	Amanda Tissawak (21762930) (author)
Άλλοι συγγραφείς:	Yarden Rosin (21762933) (author), Shirly Katz Galay (21762936) (author), Alia Qasem (21762939) (author), Michal Shahar (15266558) (author), Nirit Trabelsi (21762942) (author), Ora Furman-Schueler (21762945) (author), Steven M. Johnson (17357) (author), Anat Florentin (21762948) (author)
Έκδοση:	2025
Θέματα:	Biophysics Biochemistry Medicine Microbiology Cell Biology Genetics Pharmacology Evolutionary Biology Hematology Infectious Diseases Biological Sciences not elsewhere classified using genetic tools first replication cycle computational structural model additional targets outside previously unknown function synthesize essential biomolecules parasite death due div >< p cpn60 physically binds affect hs response apicoplast translation inhibitors apicoplast function work reveals taken together stable interface refolding safeguard plasmodium </ parasites serves organellar damage minimal control metabolic hub inactive forms immediately within heat shock evidence suggests eukaryotic cells endosymbiotic organelles directly involved conserved chaperonin close orthologues chaperonin inhibition cell nucleus caseinolytic protease balanced activities anti -<
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CPN60 is not involved in Heat Shock response.

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