| MAML3 Contributes to Induction of Malignant Phenotype of Gallbladder Cancer Through Morphogenesis Signalling Under Hypoxia. | MAML3 Contributes to Induction of Malignant Phenotype of Gallbladder Cancer Through Morphogenesis Signalling Under Hypoxia.
Na L, Onishi H, Morisaki S, Ichimiya S, Yamada Y, Masuda S, Nagao S, Koga S, Nakayama K, Imaizumi A, Oda Y, Nakamura M. | 06/30/2023 |
| Mastermind Like Transcriptional Coactivator 3 (MAML3) Drives Neuroendocrine Tumor Progression. | Mastermind Like Transcriptional Coactivator 3 (MAML3) Drives Neuroendocrine Tumor Progression.
Alzofon N, Koc K, Panwell K, Pozdeyev N, Marshall CB, Albuja-Cruz M, Raeburn CD, Nathanson KL, Cohen DL, Wierman ME, Kiseljak-Vassiliades K, Fishbein L., Free PMC Article | 02/12/2022 |
| RBPJ and MAML3 could be new therapeutic targets for SCLC. | RBPJ and MAML3: Potential Therapeutic Targets for Small Cell Lung Cancer.
Onishi H, Ichimiya S, Yanai K, Umebayashi M, Nakamura K, Yamasaki A, Imaizumi A, Nagai S, Murahashi M, Ogata H, Morisaki T. | 08/4/2018 |
| PTTG1IP and MAML3 are associated with BHR severity in adult asthma. The relevance of these genes is supported by the eQTL analyses and co-expression of PTTG1lP with vimentin and E-cadherin1, and MAML3 with MAML2. | PTTG1IP and MAML3, novel genomewide association study genes for severity of hyperresponsiveness in adult asthma.
Nieuwenhuis MA, Vonk JM, Himes BE, Sarnowski C, Minelli C, Jarvis D, Bouzigon E, Nickle DC, Laviolette M, Sin D, Weiss ST, van den Berge M, Koppelman GH, Postma DS. | 12/9/2017 |
| These findings indicate that the miR-2392-MAML3/WHSC1-Slug/Twist1 regulatory axis plays a critical role in GC metastasis. | MiR-2392 suppresses metastasis and epithelial-mesenchymal transition by targeting MAML3 and WHSC1 in gastric cancer.
Li J, Li T, Lu Y, Shen G, Guo H, Wu J, Lei C, Du F, Zhou F, Zhao X, Nie Y, Fan D. | 10/14/2017 |
| Results show that overexpression of MAML3 confers resistance to retinoic acid in multiple neuroblastoma cell lines. | Mastermind-Like 3 Controls Proliferation and Differentiation in Neuroblastoma.
Heynen GJ, Nevedomskaya E, Palit S, Jagalur Basheer N, Lieftink C, Schlicker A, Zwart W, Bernards R, Bajpe PK. | 08/12/2017 |
| These results suggest that PSK suppresses Hedgehog signaling through down-regulation of MAML3 and RBPJ transcription under hypoxia, inhibiting the induction of a malignant phenotype in pancreatic cancer. Our results may lead to development of new treatments for refractory pancreatic cancer using PSK as a Hedgehog inhibitor | Protein-bound Polysaccharide-K Inhibits Hedgehog Signaling Through Down-regulation of MAML3 and RBPJ Transcription Under Hypoxia, Suppressing the Malignant Phenotype in Pancreatic Cancer.
Yamasaki A, Onishi H, Imaizumi A, Kawamoto M, Fujimura A, Oyama Y, Katano M. | 01/28/2017 |
| The present study further expands the genetic spectrum of small blue round cell tumors, with 2 novel fusions, BCOR-MAML3 and ZC3H7B-BCOR, identified | Novel BCOR-MAML3 and ZC3H7B-BCOR Gene Fusions in Undifferentiated Small Blue Round Cell Sarcomas.
Specht K, Zhang L, Sung YS, Nucci M, Dry S, Vaiyapuri S, Richter GH, Fletcher CD, Antonescu CR., Free PMC Article | 08/6/2016 |
| Suggest that hypoxia promotes SMO transcription through upregulation of MAML3 and RBPJ to induce proliferation, invasiveness and tumorigenesis in pancreatic cancer. | Hypoxia but not normoxia promotes Smoothened transcription through upregulation of RBPJ and Mastermind-like 3 in pancreatic cancer.
Onishi H, Yamasaki A, Kawamoto M, Imaizumi A, Katano M. | 06/28/2016 |
| Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator) | Personalized smoking cessation: interactions between nicotine dose, dependence and quit-success genotype score.
Rose JE, Behm FM, Drgon T, Johnson C, Uhl GR., Free PMC Article | 06/30/2010 |
| Identification of new human proteins defines a family that consists of positive regulators for notch signaling | Identification of new human mastermind proteins defines a family that consists of positive regulators for notch signaling.
Lin SE, Oyama T, Nagase T, Harigaya K, Kitagawa M. | 01/21/2010 |