c-Rel


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c-Rel

A member of the NF-kappaB family of transcription factors encoded by REL on chromosome 2p13-p12, which is distinguished by the presence of an N-terminal Rel homology domain.

Significance
c-Rel overexpression causes downregulation of EPHB2 (an ephrin receptor tyrosine kinase in the intestine), and is associated with a poor prognosis in colorectal carcinoma.
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References in periodicals archive ?
The c-Rel Transcription Factor and B-cell Proliferation: a Deal with the Devil.
Mouse Mammary Tumor Virus C-rel Transgenic Mice Develop Mammary Tumors.
TCR and CD28 stimulation results in activation and nuclear entry of c-Rel. In contrast, Foxo protein that are constitutively present in the nucleus are phosphorylated and inactivated by the PI3K/Akt signalling axis downstream of TCR.
Grumont et al., "c-Rel is required for the development of thymic Foxp3+ CD4 regulatory T cells," Journal of Experimental Medicine, vol.
As an example, the observation in primary mouse keratinocytes that c-Rel acts downstream of [DELTA]Np63[alpha] in modulating keratinocyte growth regulation led to a further novel observation that c-Rel levels are enhanced in primary HNSCC of humans and links this protein accumulation to altered NF[kappa]B/c-Rel activity in human head and neck squamous cell cancer cells [134].
Varigos et al., "The transcription factors c-rel and RelA control epidermal development and homeostasis in embryonic and adult skin via distinct mechanisms," Molecular and Cellular Biology, vol.
No supershifting occurred, so band elimination was the indicator for the presence of c-Rel in the HMEC-1 extracts (Fig.
Band 2 composition, appears to be more complex, however, with RelA, p50, and c-Rel present at all time points.
These NF-[kappa]B/Rel subunits are p65/Rel-A, c-Rel, Rel-B, p105/NF-[kappa]B1 (which can be processed to p50), and p100/NF-[kappa]B2 (which can be processed to p52).
californicus induces the nuclear binding activity of a well-known transcription factor NF-[kappa]B, including one complex with c-Rel and some unidentified subunits.
Indeed, recent gene knockout studies provided convincing evidence that a deficiency in B cells occurred when the genes nfkb1 (p50/p105), nfkb2 (p52/p100), and c-rel were disrupted.