| ADAM22 acts as a novel predictive biomarker for unfavorable prognosis and facilitates metastasis via PI3K/AKT signaling pathway in nasopharyngeal carcinoma. | ADAM22 acts as a novel predictive biomarker for unfavorable prognosis and facilitates metastasis via PI3K/AKT signaling pathway in nasopharyngeal carcinoma.
Xu K, Jiang P, Chen Z, Gu X, Zhang T. | 04/16/2024 |
| Biallelic ADAM22 pathogenic variants cause progressive encephalopathy and infantile-onset refractory epilepsy. | Biallelic ADAM22 pathogenic variants cause progressive encephalopathy and infantile-onset refractory epilepsy.
van der Knoop MM, Maroofian R, Fukata Y, van Ierland Y, Karimiani EG, Lehesjoki AE, Muona M, Paetau A, Miyazaki Y, Hirano Y, Selim L, de França M, Fock RA, Beetz C, Ruivenkamp CAL, Eaton AJ, Morneau-Jacob FD, Sagi-Dain L, Shemer-Meiri L, Peleg A, Haddad-Halloun J, Kamphuis DJ, Peeters-Scholte CMPCD, Kurul SH, Horvath R, Lochmüller H, Murphy D, Waldmüller S, Spranger S, Overberg D, Muir AM, Rad A, Vona B, Abdulwahad F, Maddirevula S, Povolotskaya IS, Voinova VY, Gowda VK, Srinivasan VM, Alkuraya FS, Mefford HC, Alfadhel M, Haack TB, Striano P, Severino M, Fukata M, Hilhorst-Hofstee Y, Houlden H., Free PMC Article | 08/6/2022 |
| LGI3 is secreted and binds to ADAM22 via TRIF-dependent NF-kappaB pathway in response to LPS in human keratinocytes. | LGI3 is secreted and binds to ADAM22 via TRIF-dependent NF-κB pathway in response to LPS in human keratinocytes.
Lee SH, Kwon NS, Baek KJ, Yun HY, Kim DS. | 07/31/2021 |
| ADAM22/LGI1 complex as a new actionable target for breast cancer brain metastasis. | ADAM22/LGI1 complex as a new actionable target for breast cancer brain metastasis.
Charmsaz S, Doherty B, Cocchiglia S, Varešlija D, Marino A, Cosgrove N, Marques R, Priedigkeit N, Purcell S, Bane F, Bolger J, Byrne C, O'Halloran PJ, Brett F, Sheehan K, Brennan K, Hopkins AM, Keelan S, Jagust P, Madden S, Martinelli C, Battaglini M, Oesterreich S, Lee AV, Ciofani G, Hill ADK, Young LS., Free PMC Article | 02/27/2021 |
| the LGI1-ADAM22 complex functions as the trans-synaptic machinery for precise synaptic transmission | Structural basis of epilepsy-related ligand-receptor complex LGI1-ADAM22.
Yamagata A, Miyazaki Y, Yokoi N, Shigematsu H, Sato Y, Goto-Ito S, Maeda A, Goto T, Sanbo M, Hirabayashi M, Shirouzu M, Fukata Y, Fukata M, Fukai S., Free PMC Article | 12/22/2018 |
| ADAM22 is critically involved in miR-449a-reduced tamoxifen resistance of estrogen receptor-positive breast cancer cells as a direct target of miR-449a. | miR-449a Suppresses Tamoxifen Resistance in Human Breast Cancer Cells by Targeting ADAM22.
Li J, Lu M, Jin J, Lu X, Xu T, Jin S. | 11/3/2018 |
| these results support the existence of a second mechanism, alternative to inhibition of protein secretion, by which ADLTE-causing LGI1 mutations exert their loss-of-function effect extracellularly, and suggest that interactions of LGI1 with both ADAM22 and ADAM23 play an important role in the molecular mechanisms leading to utosomal dominant lateral temporal epilepsy | Secretion-Positive LGI1 Mutations Linked to Lateral Temporal Epilepsy Impair Binding to ADAM22 and ADAM23 Receptors.
Dazzo E, Leonardi E, Belluzzi E, Malacrida S, Vitiello L, Greggio E, Tosatto SC, Nobile C., Free PMC Article | 05/13/2017 |
| Disruption of LGI1-ADAM22 interaction reduces synaptic AMPA receptors in hippocampal neurons. | Autoantibodies to epilepsy-related LGI1 in limbic encephalitis neutralize LGI1-ADAM22 interaction and reduce synaptic AMPA receptors.
Ohkawa T, Fukata Y, Yamasaki M, Miyazaki T, Yokoi N, Takashima H, Watanabe M, Watanabe O, Fukata M., Free PMC Article | 01/11/2014 |
| Data suggest that ADAM22 plays roles in cell differentiation, cell migration, and resistance to endocrine therapy in breast cancer; ADAM22 may serve as biomarker for poor disease-free survival in breast cancer patients. [REVIEW] | ADAM22 as a prognostic and therapeutic drug target in the treatment of endocrine-resistant breast cancer.
Bolger JC, Young LS. | 12/14/2013 |
| findings suggest that SRC-1 switches steroid-responsive tumors to a steroid-resistant state in which the SRC-1 target gene ADAM22 has a critical role | Global characterization of the SRC-1 transcriptome identifies ADAM22 as an ER-independent mediator of endocrine-resistant breast cancer.
McCartan D, Bolger JC, Fagan A, Byrne C, Hao Y, Qin L, McIlroy M, Xu J, Hill AD, Gaora PÓ, Young LS., Free PMC Article | 02/25/2012 |
| 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 |
| Mutations in disintegrin domain sequence in ADAM22 gene is associted with reduced LGI4-binding abilities resulting in epilepsy. | Biological characterization of ADAM22 variants reveals the importance of a disintegrin domain sequence in cell surface expression.
Sagane K, Sugimoto H, Akaike A. | 06/28/2010 |
| Transgenic leucine-rich glioma-inactivated 4 (Lgi4) and transgenic Adam22 proteins are both expressed in Schwann cells as well as in sensory neurons; binding of Lgi4 to axonal Adam22 is required on axons to drive myelin formation. | Adam22 is a major neuronal receptor for Lgi4-mediated Schwann cell signaling.
Ozkaynak E, Abello G, Jaegle M, van Berge L, Hamer D, Kegel L, Driegen S, Sagane K, Bermingham JR Jr, Meijer D., Free PMC Article | 04/12/2010 |
| The pro domains of ADAMs are expressed as two subdomains. The most N-terminal subdomain (ADAM22-P(N)) was found to be susceptible to proteolysis and was required for folding stability of the second subdomain (ADAM22-P(C)). | Expression, purification and insights into structure and folding of the ADAM22 pro domain.
Sørensen HP, Jacobsen J, Nielbo S, Poulsen FM, Wewer UM. | 01/21/2010 |
| Observational study of gene-disease association. (HuGE Navigator) | Polymorphisms in genes involved in neurodevelopment may be associated with altered brain morphology in schizophrenia: preliminary evidence.
Gregório SP, Sallet PC, Do KA, Lin E, Gattaz WF, Dias-Neto E. | 01/11/2009 |
| our results suggest that neither ADAM22 nor any of the three Kv1 channel genes are major causative genes for ADLTE. | Autosomal dominant lateral temporal epilepsy: absence of mutations in ADAM22 and Kv1 channel genes encoding LGI1-associated proteins.
Diani E, Di Bonaventura C, Mecarelli O, Gambardella A, Elia M, Bovo G, Bisulli F, Pinardi F, Binelli S, Egeo G, Castellotti B, Striano P, Striano S, Bianchi A, Ferlazzo E, Vianello V, Coppola G, Aguglia U, Tinuper P, Giallonardo AT, Michelucci R, Nobile C. | 01/21/2010 |
| This study indicated ADAM22 gene is probably not a major gene for this epilepsy syndrome. | Absence of mutations in the LGI1 receptor ADAM22 gene in autosomal dominant lateral temporal epilepsy.
Chabrol E, Gourfinkel-An I, Scheffer IE, Picard F, Couarch P, Berkovic SF, McMahon JM, Bajaj N, Mota-Vieira L, Mota R, Trouillard O, Depienne C, Baulac M, LeGuern E, Baulac S. | 01/21/2010 |
| Differential coding potential of ADAM22 mRNAs. | Differential coding potential of ADAM22 mRNAs.
Gödde NJ, D'Abaco GM, Paradiso L, Novak U. | 01/21/2010 |
| ADAM22, a brain-specific cell surface protein, mediates growth inhibition using an integrin dependent pathway. It is expressed in normal brain but not in high-grade gliomas. | ADAM22, expressed in normal brain but not in high-grade gliomas, inhibits cellular proliferation via the disintegrin domain.
D'Abaco GM, Ng K, Paradiso L, Godde NJ, Kaye A, Novak U. | 01/21/2010 |
| demonstrated a functional role for ADAM22/14-3-3 in cell adhesion and spreading | ADAM22 plays an important role in cell adhesion and spreading with the assistance of 14-3-3.
Zhu P, Sang Y, Xu H, Zhao J, Xu R, Sun Y, Xu T, Wang X, Chen L, Feng H, Li C, Zhao S. | 01/21/2010 |
| role for the 14-3-3zeta/ADAM 22 association in the regulation of cell adhesion and related signaling events | The interaction between ADAM 22 and 14-3-3zeta: regulation of cell adhesion and spreading.
Zhu Pc, Sun Y, Xu R, Sang Y, Zhao J, Liu G, Cai L, Li C, Zhao S. | 01/21/2010 |