| CBLL1 promotes endometrial stromal cell senescence via inhibiting PTEN in recurrent spontaneous abortion. | CBLL1 promotes endometrial stromal cell senescence via inhibiting PTEN in recurrent spontaneous abortion.
Liu X, Wei X, Wu J, Xu Y, Hu J, Qin C, Chen C, Lin Y. | 08/14/2024 |
| Stratification of Colorectal Patients Based on Survival Analysis Shows the Value of Consensus Molecular Subtypes and Reveals the CBLL1 Gene as a Biomarker of CMS2 Tumours. | Stratification of Colorectal Patients Based on Survival Analysis Shows the Value of Consensus Molecular Subtypes and Reveals the CBLL1 Gene as a Biomarker of CMS2 Tumours.
Alfonsín G, Berral-González A, Rodríguez-Alonso A, Quiroga M, De Las Rivas J, Figueroa A., Free PMC Article | 02/28/2024 |
| CBLL1 is hypomethylated and correlates with cortical thickness in transgender men before gender affirming hormone treatment. | CBLL1 is hypomethylated and correlates with cortical thickness in transgender men before gender affirming hormone treatment.
Fernández R, Zubiaurre-Elorza L, Santisteban A, Ojeda N, Collet S, Kiyar M, T'Sjoen G, Mueller SC, Guillamon A, Pásaro E., Free PMC Article | 01/8/2024 |
| Role of the E3 ubiquitin-ligase Hakai in intestinal inflammation and cancer bowel disease. | Role of the E3 ubiquitin-ligase Hakai in intestinal inflammation and cancer bowel disease.
Roca-Lema D, Quiroga M, Khare V, Díaz-Díaz A, Barreiro-Alonso A, Rodríguez-Alonso A, Concha Á, Romay G, Cerdán ME, Gasche C, Figueroa A., Free PMC Article | 10/29/2022 |
| Downregulation of long non-coding RNA XIST inhibits cell proliferation, migration, invasion and EMT by regulating miR-212-3p/CBLL1 axis in non-small cell lung cancer cells. | Downregulation of long non-coding RNA XIST inhibits cell proliferation, migration, invasion and EMT by regulating miR-212-3p/CBLL1 axis in non-small cell lung cancer cells.
Qiu HB, Yang K, Yu HY, Liu M. | 12/19/2020 |
| Study have demonstrated that CBLL1 is highly expressed in non-small lung cancer (NSCLC) cancer tissues compared with corresponding normal lung tissues, and correlated with tumor size. Moreover, CBLL1 promotes the cell proliferation by inducing the G0/G1-S transition and cell invasion by increasing degradation of extracellular matrices of NSCLC cells. | CBLL1 is highly expressed in non-small cell lung cancer and promotes cell proliferation and invasion.
Hui L, Zhang S, Wudu M, Ren H, Xu Y, Zhang Q, Qiu X., Free PMC Article | 06/27/2020 |
| we have detected the presence of micrometastasis in the lung mice, further confirming Hakai role during tumour metastasis in vivo. These results lead to the consideration of Hakai as a potential new therapeutic target to block tumour development and metastasis | Hakai overexpression effectively induces tumour progression and metastasis in vivo.
Castosa R, Martinez-Iglesias O, Roca-Lema D, Casas-Pais A, Díaz-Díaz A, Iglesias P, Santamarina I, Graña B, Calvo L, Valladares-Ayerbes M, Concha Á, Figueroa A., Free PMC Article | 09/14/2019 |
| The present study demonstrated for the first time that knockdown of Hakai inhibited the proliferation, migration and invasion of nonsmallcell lung cancer cells, and sensitized nonsmallcell lung cancer cells to cisplatin. | E3 ubiquitin ligase Hakai regulates cell growth and invasion, and increases the chemosensitivity to cisplatin in non‑small‑cell lung cancer cells.
Liu Z, Wu Y, Tao Z, Ma L. | 10/13/2018 |
| findings suggest that the E3 ubiquitin-ligase, such as Hakai, may be a better target than proteasome for using novel specific inhibitors in tumor subtypes that follow EMT. | Proteomic Analysis of the E3 Ubiquitin-Ligase Hakai Highlights a Role in Plasticity of the Cytoskeleton Dynamics and in the Proteasome System.
Díaz-Díaz A, Casas-Pais A, Calamia V, Castosa R, Martinez-Iglesias O, Roca-Lema D, Santamarina I, Valladares-Ayerbes M, Calvo L, Chantada V, Figueroa A. | 05/19/2018 |
| These results suggest that stabilization of delta-catenin by Hakai is dependent on Src. | Hakai, an E3-ligase for E-cadherin, stabilizes δ-catenin through Src kinase.
Shrestha H, Ryu T, Seo YW, Park SY, He Y, Dai W, Park E, Simkhada S, Kim H, Lee K, Kim K. | 12/2/2017 |
| these observations suggest that the dimeric architecture of the HYB domain is essential for the phosphotyrosine-binding property of Hakai. | Dimeric switch of Hakai-truncated monomers during substrate recognition: insights from solution studies and NMR structure.
Mukherjee M, Jing-Song F, Ramachandran S, Guy GR, Sivaraman J., Free PMC Article | 02/21/2015 |
| By lowering Hakai abundance, miR-203 also reduces Hakai-regulated-cell division. | miR-203 regulates cell proliferation through its influence on Hakai expression.
Abella V, Valladares M, Rodriguez T, Haz M, Blanco M, Tarrío N, Iglesias P, Aparicio LA, Figueroa A., Free PMC Article | 06/15/2013 |
| Hakai dimerization allows the formation of a phosphotyrosine-binding pocket that recognizes specific phosphorylated tyrosines and flanking acidic amino acids of Src substrates, such as E-cadherin, cortactin and DOK1. | Structure of a novel phosphotyrosine-binding domain in Hakai that targets E-cadherin.
Mukherjee M, Chow SY, Yusoff P, Seetharaman J, Ng C, Sinniah S, Koh XW, Asgar NF, Li D, Yim D, Jackson RA, Yew J, Qian J, Iyu A, Lim YP, Zhou X, Sze SK, Guy GR, Sivaraman J., Free PMC Article | 05/5/2012 |
| Hakai mediates E-cadherin ubiquitination and degradation triggered by Slit-Robo signaling during colorectal epithelial cell carcinogenesis. | Slit-Robo signaling induces malignant transformation through Hakai-mediated E-cadherin degradation during colorectal epithelial cell carcinogenesis.
Zhou WJ, Geng ZH, Chi S, Zhang W, Niu XF, Lan SJ, Ma L, Yang X, Wang LJ, Ding YQ, Geng JG., Free PMC Article | 10/22/2011 |
| Together, these data do not support a requirement for CBLL1 during flavivirus entry and rather suggest an essential role of the ubiquitin/proteasome pathway for flavivirus genome amplification. | Appraising the roles of CBLL1 and the ubiquitin/proteasome system for flavivirus entry and replication.
Fernandez-Garcia MD, Meertens L, Bonazzi M, Cossart P, Arenzana-Seisdedos F, Amara A., Free PMC Article | 04/16/2011 |
| Results suggest that Hakai is a novel corepressor of ERalpha and may play a negative role in the development and progression of breast cancers. | Hakai acts as a coregulator of estrogen receptor alpha in breast cancer cells.
Gong EY, Park E, Lee K., Free PMC Article | 02/26/2011 |
| 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 |
| Results suggest that Hakai is an important regulator of cell proliferation and that Hakai may be an oncoprotein and a potential molecular target for cancer treatment. | Novel roles of hakai in cell proliferation and oncogenesis.
Figueroa A, Kotani H, Toda Y, Mazan-Mamczarz K, Mueller EC, Otto A, Disch L, Norman M, Ramdasi RM, Keshtgar M, Gorospe M, Fujita Y., Free PMC Article | 02/22/2010 |