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
Cytochrome c
(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!
=== Inhibition of apoptosis === One of the ways cell apoptosis is activated is by release of cytochrome c from the mitochondria into cytosol. A study has shown that cells are able to protect themselves from apoptosis by blocking the release of cytochrome c using Bcl-x<sub>L</sub>.<ref>{{Cite journal |vauthors=Kharbanda S, Pandey P, Schofield L, Israels S, Roncinske R, Yoshida K, Bharti A, Yuan ZM, Saxena S, Weichselbaum R, Nalin C, Kufe D |date=June 1997 |title=Role for Bcl-xL as an inhibitor of cytosolic cytochrome C accumulation in DNA damage-induced apoptosis |journal=Proceedings of the National Academy of Sciences of the United States of America |volume=94 |issue=13 |pages=6939–42 |bibcode=1997PNAS...94.6939K |doi=10.1073/pnas.94.13.6939 |pmc=21263 |pmid=9192670 |doi-access=free}}</ref> Another way that cells can control apoptosis is by phosphorylation of Tyr48, which turns cytochrome c into an anti-apoptotic switch.<ref>{{Cite journal |vauthors=García-Heredia JM, Díaz-Quintana A, Salzano M, Orzáez M, Pérez-Payá E, Teixeira M, De la Rosa MA, Díaz-Moreno I |date=December 2011 |title=Tyrosine phosphorylation turns alkaline transition into a biologically relevant process and makes human cytochrome c behave as an anti-apoptotic switch |journal=[[Journal of Biological Inorganic Chemistry]] |volume=16 |issue=8 |pages=1155–68 |doi=10.1007/s00775-011-0804-9 |pmid=21706253 |s2cid=24156094}}</ref>
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)