| A recurrent missense variant in the E3 ubiquitin ligase substrate recognition subunit FEM1B causes a rare syndromic neurodevelopmental disorder. | A recurrent missense variant in the E3 ubiquitin ligase substrate recognition subunit FEM1B causes a rare syndromic neurodevelopmental disorder.
Lecoquierre F, Punt AM, Ebstein F, Wallaard I, Verhagen R, Studencka-Turski M, Duffourd Y, Moutton S, Tran Mau-Them F, Philippe C, Dean J, Tennant S, Brooks AS, van Slegtenhorst MA, Jurgens JA, Barry BJ, Chan WM, England EM, Martinez Ojeda M, Engle EC, Robson CD, Morrow M, Innes AM, Lamont R, Sanderson M, Krüger E, Thauvin C, Distel B, Faivre L, Elgersma Y, Vitobello A., Free PMC Article | 10/30/2024 |
| Structural insights into the ubiquitylation strategy of the oligomeric CRL2[FEM1B] E3 ubiquitin ligase. | Structural insights into the ubiquitylation strategy of the oligomeric CRL2(FEM1B) E3 ubiquitin ligase.
Dai Z, Liang L, Wang W, Zuo P, Yu S, Liu Y, Zhao X, Lu Y, Jin Y, Zhang F, Ding D, Deng W, Yin Y., Free PMC Article | 03/18/2024 |
| Structural insights into SMCR8 C-degron recognition by FEM1B. | Structural insights into SMCR8 C-degron recognition by FEM1B.
Zhao S, Ru W, Chen X, Liao S, Zhu Z, Zhang J, Xu C. | 08/14/2021 |
| Molecular basis for ubiquitin ligase CRL2(FEM1C)-mediated recognition of C-degron. | Molecular basis for ubiquitin ligase CRL2(FEM1C)-mediated recognition of C-degron.
Yan X, Wang X, Li Y, Zhou M, Li Y, Song L, Mi W, Min J, Dong C. | 04/3/2021 |
| Molecular basis for arginine C-terminal degron recognition by Cul2(FEM1) E3 ligase. | Molecular basis for arginine C-terminal degron recognition by Cul2(FEM1) E3 ligase.
Chen X, Liao S, Makaros Y, Guo Q, Zhu Z, Krizelman R, Dahan K, Tu X, Yao X, Koren I, Xu C. | 04/3/2021 |
| FEM1 proteins are ancient regulators of Stem-Loop Binding Protein. | FEM1 proteins are ancient regulators of SLBP degradation.
Dankert JF, Pagan JK, Starostina NG, Kipreos ET, Pagano M., Free PMC Article | 06/24/2017 |
| These findings have implications for understanding the cellular functions of Fem1b, and the regulation of Gli1 oncoprotein activity. | Fem1b promotes ubiquitylation and suppresses transcriptional activity of Gli1.
Gilder AS, Chen YB, Jackson RJ 3rd, Jiang J, Maher JF., Free PMC Article | 05/3/2014 |
| Observational study of gene-disease association, gene-gene interaction, gene-environment interaction, and genetic testing. (HuGE Navigator) | Integrative predictive model of coronary artery calcification in atherosclerosis.
McGeachie M, Ramoni RL, Mychaleckyj JC, Furie KL, Dreyfuss JM, Liu Y, Herrington D, Guo X, Lima JA, Post W, Rotter JI, Rich S, Sale M, Ramoni MF., Free PMC Article | 04/7/2010 |
| the proapoptotic protein Fem1b is downregulated by the proteasome in malignant colon cancer cells and mediates proteasome inhibitor-induced apoptosis of these cells | Fem1b, a proapoptotic protein, mediates proteasome inhibitor-induced apoptosis of human colon cancer cells.
Subauste MC, Sansom OJ, Porecha N, Raich N, Du L, Maher JF. | 02/22/2010 |
| FEM1B is required for Rad9 recruitment and CHK1 activation in response to replication stress. | Human FEM1B is required for Rad9 recruitment and CHK1 activation in response to replication stress.
Sun TP, Shieh SY. | 01/21/2010 |
| This study presents evidence suggesting a role for FEM1A and FEM1B in the pathogenesis of polycystic ovary syndrome. Only FEM1B variants were associated with insulin-related traits in PCOS women. | FEM1A and FEM1B: novel candidate genes for polycystic ovary syndrome.
Goodarzi MO, Maher JF, Cui J, Guo X, Taylor KD, Azziz R, Goodarzi MO, Maher JF, Cui J, Guo X, Taylor KD, Azziz R., Free PMC Articles: PMC2583941, PMC2583941 | 01/21/2010 |
| Observational study of gene-disease association. (HuGE Navigator) | See all PubMed (2) articlesFamily-based analysis of candidate genes for polycystic ovary syndrome.
Ewens KG, Stewart DR, Ankener W, Urbanek M, McAllister JM, Chen C, Baig KM, Parker SC, Margulies EH, Legro RS, Dunaif A, Strauss JF 3rd, Spielman RS. FEM1A and FEM1B: novel candidate genes for polycystic ovary syndrome.
Goodarzi MO, Maher JF, Cui J, Guo X, Taylor KD, Azziz R, Goodarzi MO, Maher JF, Cui J, Guo X, Taylor KD, Azziz R. | 09/10/2008 |