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the LGI1-ADAM22 complex functions as the trans-synaptic machinery for precise synaptic transmission
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ADAM22 is critically involved in miR-449a-reduced tamoxifen resistance of estrogen receptor-positive breast cancer cells as a direct target of miR-449a.
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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
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Disruption of LGI1-ADAM22 interaction reduces synaptic AMPA receptors in hippocampal neurons.
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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]
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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
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Mutations in disintegrin domain sequence in ADAM22 gene is associted with reduced LGI4-binding abilities resulting in epilepsy.
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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.
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role for the 14-3-3zeta/ADAM 22 association in the regulation of cell adhesion and related signaling events
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demonstrated a functional role for ADAM22/14-3-3 in cell adhesion and spreading
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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.
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This study indicated ADAM22 gene is probably not a major gene for this epilepsy syndrome.
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Differential coding potential of ADAM22 mRNAs.
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our results suggest that neither ADAM22 nor any of the three Kv1 channel genes are major causative genes for ADLTE.
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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)).