Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Signal transduction
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
===Temperature=== {{Main|Thermoception}} The sensing of temperature in cells is known as thermoception and is primarily mediated by [[transient receptor potential channel]]s.<ref name="Sengupta">{{Cite journal |vauthors=Sengupta P, Garrity P |date=April 2013 |title=Sensing temperature |journal=Current Biology |volume=23 |issue=8 |pages=R304-7 |doi=10.1016/j.cub.2013.03.009 |pmc=3685181 |pmid=23618661}}</ref> Additionally, animal cells contain a conserved mechanism to prevent high temperatures from causing cellular damage, the [[heat-shock response]]. Such response is triggered when high temperatures cause the dissociation of inactive [[HSF1]] from complexes with [[heat shock proteins]] [[Hsp40]]/[[Hsp70]] and [[Hsp90]]. With help from the [[ncRNA]] ''hsr1'', HSF1 then trimerizes, becoming active and upregulating the expression of its target genes.<ref>{{Cite journal |vauthors=Shamovsky I, Ivannikov M, Kandel ES, Gershon D, Nudler E |date=March 2006 |title=RNA-mediated response to heat shock in mammalian cells |journal=Nature |volume=440 |issue=7083 |pages=556β60 |bibcode=2006Natur.440..556S |doi=10.1038/nature04518 |pmid=16554823 |s2cid=4311262}}</ref> Many other thermosensory mechanisms exist in both [[prokaryotes]] and [[eukaryotes]].<ref name="Sengupta" />
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)