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Sequential posttranslational modifications regulate PKC degradation
Sequential posttranslational modifications regulate PKC degradation
δ/ω-Plectoxin-Pt1a
δ/ω-Plectoxin-Pt1a
Cellular and molecular responses to acute cocaine treatment in neuronal-like N2a cells
Cellular and molecular responses to acute cocaine treatment in neuronal-like N2a cells
Intracellular regions of the Eag potassium channel play a critical role in generation of voltage-dependent currents.
Intracellular regions of the Eag potassium channel play a critical role in generation of voltage-dependent currents.
δ/ω-Plectoxin-Pt1a
δ/ω-Plectoxin-Pt1a
Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice.
Inhibition of 14-3-3 Proteins Leads to Schizophrenia-Related Behavioral Phenotypes and Synaptic Defects in Mice.
14-3-3 protein targets misfolded chaperone-associated proteins to aggresomes.
14-3-3 protein targets misfolded chaperone-associated proteins to aggresomes.
Sequential posttranslational modifications regulate PKC degradation.
Sequential posttranslational modifications regulate PKC degradation.
Intracellular linkers are involved in Mg2+-dependent modulation of the Eag potassium channel.
Intracellular linkers are involved in Mg2+-dependent modulation of the Eag potassium channel.
Algorithms for Factoring Linear Recurrence Operators
Algorithms for Factoring Linear Recurrence Operators
14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.
14-3-3τ promotes surface expression of Cav2.2 (α1B) Ca2+ channels.
14-3-3 proteins are required for hippocampal long-term potentiation and associative learning and memory.
14-3-3 proteins are required for hippocampal long-term potentiation and associative learning and memory.
14-3-3 and aggresome formation
14-3-3 and aggresome formation
14-3-3 proteins in neurological disorders.
14-3-3 proteins in neurological disorders.
14-3-3 Proteins in Glutamatergic Synapses.