This shows you the differences between two versions of the page.
Next revision | Previous revision | ||
kedrov_et_al_2019 [2019/10/11 20:05] floyd created |
kedrov_et_al_2019 [2019/10/11 20:09] floyd |
||
---|---|---|---|
Line 1: | Line 1: | ||
===Kedrov et al. 2019=== | ===Kedrov et al. 2019=== | ||
Kedrov, A. V., Durymanov, M., & Anokhin, K. V. (2019). The Arc gene: Retroviral heritage in cognitive functions. // | Kedrov, A. V., Durymanov, M., & Anokhin, K. V. (2019). The Arc gene: Retroviral heritage in cognitive functions. // | ||
+ | |||
+ | ==Links== | ||
+ | * https:// | ||
+ | * https:// | ||
+ | * {{private: | ||
+ | |||
+ | ==Abstract== | ||
+ | Stabilization of neuronal plastic changes is mediated by transient gene expression, including transcription of the activity-regulated cytoskeleton-associated gene (Arc), also known as Arg 3.1. Arc is implicated in several types of synaptic plasticity, including synaptic scaling, long-term potentiation, | ||
+ | |||
+ | ==Highlights== | ||
+ | * Immediate early gene Arc expression is crucial for animal learning and memory. | ||
+ | * Learning-induced Arc mRNA and protein accumulate at dendrites and play a role in long-term synaptic plasticity. | ||
+ | * Arc has a viral origin, is capable of forming capsid-like structures and can transfect neighboring cells with its own mRNA. | ||
+ | * This Arc features raise new intriguing questions about the role of this traffic in neuronal plasticity and memory formation. | ||
+ | * The ability of Arc to form functional capsid-like structures can be used to develop new research and therapeutic tools. | ||
+ | |||
+ | {{tag> |