| Cell adhesion molecule 4 suppresses cell growth and metastasis by inhibiting the Akt signaling pathway in non-small cell lung cancer. | Cell adhesion molecule 4 suppresses cell growth and metastasis by inhibiting the Akt signaling pathway in non-small cell lung cancer.
Luo F, Zhao Y, Liu J. | 12/26/2020 |
| There was a significant association between RNase 5 and histological differentiation in colon adenocarcinomas, but no association between RNase 5 and Necl 4 in gastric or colon adenocarcinomas | Necl 4 and RNase 5 Are Important Biomarkers for Gastric and Colon Adenocarcinomas.
Sayar İ, Gökçe A, Demirtas L, Eken H, Çimen FK, Çimen O., Free PMC Article | 03/31/2018 |
| Low CADM4 expression is associated with bone marrow metastasis in neuroblastoma. | Neuroblastoma cells undergo transcriptomic alterations upon dissemination into the bone marrow and subsequent tumor progression.
Rifatbegovic F, Frech C, Abbasi MR, Taschner-Mandl S, Weiss T, Schmidt WM, Schmidt I, Ladenstein R, Ambros IM, Ambros PF., Free PMC Article | 12/16/2017 |
| The results suggest that Necl-4 enhances VEGF-induced activation of PLCgamma-c-Raf-MEK-ERK pathway without affecting the phosphorylation and internalization of VEGFR2. | Necl-4 enhances the PLCγ-c-Raf-MEK-ERK pathway without affecting internalization of VEGFR2.
Yamana S, Tokiyama A, Fujita H, Terao Y, Horibe S, Sasaki N, Satomi-Kobayashi S, Hirata KI, Rikitake Y. | 09/30/2017 |
| Necl-4 serves as a novel regulator for contact inhibition of cell movement and proliferation cooperatively with the VEGF receptor and PTPN13 | The Cell Adhesion Molecule Necl-4/CADM4 Serves as a Novel Regulator for Contact Inhibition of Cell Movement and Proliferation.
Yamana S, Tokiyama A, Mizutani K, Hirata K, Takai Y, Rikitake Y., Free PMC Article | 02/6/2016 |
| results indicate that Necl-4 serves as a tumor suppressor by inhibiting the ErbB2/ErbB3 signaling and hemidesmosome disassembly | Interaction of Necl-4/CADM4 with ErbB3 and integrin α6 β4 and inhibition of ErbB2/ErbB3 signaling and hemidesmosome disassembly.
Sugiyama H, Mizutani K, Kurita S, Okimoto N, Shimono Y, Takai Y. | 10/4/2014 |
| Loss or decrease of CADM4 expression seems to play an important role in breast cancer invasiveness, and it is associated with poorer biological parameters. | Clinicopathological significance of CADM4 expression in invasive ductal carcinoma of the breast.
Jang SM, Sim J, Han H, Ahn HI, Kim H, Yi K, Jun YJ, Rehman A, Chung MS, Jang K, Paik SS. | 10/26/2013 |
| Cadm4 regulates the growth of the myelin unit and the organization of the underlying axonal membrane. | Genetic deletion of Cadm4 results in myelin abnormalities resembling Charcot-Marie-Tooth neuropathy.
Golan N, Kartvelishvily E, Spiegel I, Salomon D, Sabanay H, Rechav K, Vainshtein A, Frechter S, Maik-Rachline G, Eshed-Eisenbach Y, Momoi T, Peles E., Free PMC Article | 10/19/2013 |
| CADM4, as well as 4.1B is expressed specifically in human proximal tubules. | Aberrations of a cell adhesion molecule CADM4 in renal clear cell carcinoma.
Nagata M, Sakurai-Yageta M, Yamada D, Goto A, Ito A, Fukuhara H, Kume H, Morikawa T, Fukayama M, Homma Y, Murakami Y. | 06/2/2012 |
| Observational study and genome-wide association study of gene-disease association. (HuGE Navigator) | Genome-wide pleiotropy of osteoporosis-related phenotypes: the Framingham Study.
Karasik D, Hsu YH, Zhou Y, Cupples LA, Kiel DP, Demissie S., Free PMC Article | 04/7/2010 |
| Nec- 4 suppress the growth and tumorigenic ability of colon cancer cells. | The cell adhesion nectin-like molecules (Necl) 1 and 4 suppress the growth and tumorigenic ability of colon cancer cells.
Raveh S, Gavert N, Spiegel I, Ben-Ze'ev A. | 02/15/2010 |
| TSLL2 is expressed at the cell-cell attachment sites in the renal tubules, the transitional epithelia of the bladder, and the glandular epithelia of the prostate, and is a tumor-suppressor candidate in prostate cancer. | Cell adhesion and prostate tumor-suppressor activity of TSLL2/IGSF4C, an immunoglobulin superfamily molecule homologous to TSLC1/IGSF4.
Williams YN, Masuda M, Sakurai-Yageta M, Maruyama T, Shibuya M, Murakami Y. | 01/21/2010 |