Growing evidence indicates that the dysregulation of NFkB may be key to a number of diseases including arthritis, Alzheimer's, atherosclerosis and cancer.
Over the last 12 months Rockland has been developing a number of antibodies to the NFkB.
NFkB is widely recognised as a critical mediator of immune and inflammatory responses.
Other identified subunits include p52 (NFkB2), c-Rel, and RelB.
The p65, cRel, and RelB subunits are responsible for transactivation.
The p50 and p52 subunits possess DNA binding activity but limited ability to transactivate.
p52 has been reported to form transcriptionally active heterodimers with the NFkB subunit p65, similar to p50/p65 heterodimers.
The heterodimers of p52/p65 and p50/p65 are regulated by physical inactivation in the cytoplasm by IkB-a. IkB-a and #61472;binds to the p65 subunit, preventing nuclear localisation and DNA binding.
Low levels of p52 and p50 homodimers can also exist in cells.
Growing evidence indicates that the dysregulation of NFkB may be key to a number of diseases including arthritis and other inflammatory diseases, Alzheimer's, atherosclerosis and cancer.
Rockland has developed antibodies for all of the above targets.
