Editing CREB (section)

==Disease linkage==
Disturbance of CREB function in the brain can contribute to the development and progression of [[Huntington's disease]].

Abnormalities of a protein that interacts with the KID domain of CREB, the [[CREB-binding protein]], (CBP) is associated with [[Rubinstein–Taybi syndrome]].

There is some evidence to suggest that the under-functioning of CREB is associated with [[major depressive disorder]].<ref name="Bel">{{cite journal | last1 = Belmaker | first1 = R. H. | last2 = Agam | first2 = Galila | year = 2008 | title = Major depressive disorder | journal = New England Journal of Medicine | volume = 358 | issue = 1| pages = 55–68 | doi=10.1056/nejmra073096| pmid = 18172175 }}</ref> Depressed rats with an overexpression of CREB in the [[dentate gyrus]] behaved similarly to rats treated with antidepressants.<ref name="Blendy">{{cite journal | last1 = Blendy | first1 = JA | year = 2006 | title = The role of CREB in depression and antidepressant treatment | journal = Biol Psychiatry | volume = 59 | issue = 12| pages = 1144–50 | doi=10.1016/j.biopsych.2005.11.003| pmid = 16457782 | s2cid = 20918484 }}</ref> From post-mortem examinations it has also been shown that the cortices of patients with untreated major depressive disorder contain reduced concentrations of CREB compared to both healthy controls and patients treated with antidepressants.<ref name="Blendy" />  The function of CREB can be modulated via a signalling pathway resulting from the binding of [[serotonin]] and [[noradrenaline]] to post-synaptic G-protein coupled receptors. Dysfunction of these neurotransmitters is also implicated in major depressive disorder.<ref name="Bel" />

CREB is also thought to be involved in the growth of some types of cancer.