@article{oai:u-ryukyu.repo.nii.ac.jp:02012284,
 author = {Sarkar, Bidhan and Nishikata, Ichiro and Nakahata, Shingo and Ichikawa, Tomonaga and Shiraga, Toshiyuki and Saha, Hashi Rani and Tanaka, Yuetsu and Shimoda, Kazuya and Morishita, Kazuhiro},
 issue = {3491},
 journal = {Scientific Reports},
 month = {Mar},
 note = {Cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is identified as a novel cell surface marker for human T-cell leukemia virus (HTLV-1)-infected T cells. Adult T-cell leukemia/lymphoma (ATLL) is developed in HTLV-1-infected T-cells after a long infection period. To examine the mechanism of CADM1 overexpression in ATLL, we first identified that CADM1 is transcriptionally up-regulated by a transcriptional enhancer element through NF-κB signaling pathway. In HTLV-1-infected T-cells, CADM1 expression is dependent on HTLV-1/Tax through activation of canonical and non-canonical NF-κB; however, in ATLL cells with frequent loss of Tax expression, the activation of canonical NF-κB only enhances the CADM1 expression. Along with active mutations in signaling molecules under T-cell recepor (TCR) signaling, degradation of p47, a negative regulator of NF-κB, was essential for activation of canonical NF-κB through stabilization of NEMO (NF-κB essential modulator). The mechanism of p47 degradation is primarily dependent on activation of lysosomal-autophagy and the autophagy is activated in most of the HTLV-infected and ATLL cells, suggesting that the p47 degradation may be a first key molecular event during HTLV-1 infection to T-cells as a connector of two important signaling pathways, NF-κB and autophagy., 論文},
 title = {Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB},
 volume = {9},
 year = {2019}
}