The selective degradation of many short-lived proteins in eukaryotic cells is carried out by the ubiquitin system. In this pathway, proteins are targeted for degradation by covalent ligation to ubiquitin, a highly conserved small protein. Ubiquitin-mediated degradation of regulatory proteins plays important roles in the control of numerous processes, including cell-cycle progression, signal transduction, transcriptional regulation, receptor down-regulation, and endocytosis. The ubiquitin system has been implicated in the immune response, development, and programmed cell death. Abnormalities in ubiquitin-mediated processes have been shown to cause pathological conditions, including malignant transformation. In this review we discuss recent information on functions and mechanisms of the ubiquitin system. Since the selectivity of protein degradation is determined mainly at the stage of ligation to ubiquitin, special attention is focused on what we know, and would like to know, about the mode of action of ubiquitin-protein ligation systems and about signals in proteins recognized by these systems.

The Ubiquitin System

Brain-computer interfaces for communication and control.

Between the 1960s and 1980s, most life scientists focused their attention on studies of nucleic acids and the translation of the coded information. Protein degradation was a neglected area, conside...

The Ubiquitin-Proteasome Proteolytic Pathway: Destruction for the Sake of Construction

From the Publisher:
The old opposition of matter versus mind stubbornly persists in the way we study mind and brain. In treating cognition as problem solving, Andy Clark suggests, we may often abstract too far from the very body and world in which our brains evolved to guide us. Whereas the mental has been treated as a realm that is distinct from the body and the world, Clark forcefully attests that a key to understanding brains is to see them as controllers of embodied activity. From this paradigm shift he advances the construction of a cognitive science of the embodied mind.

/pdf/being-there-putting-brain-body-and-world-together-again-31tt4y51ml.pdf

Being There: Putting Brain, Body, and World Together Again

One of the most remarkable aspects of an animal's behavior is the ability to modify that behavior by learning, an ability that reaches its highest form in human beings. For me, learning and memory have proven to be endlessly fascinating mental processes because they address one of the fundamental features of human activity: our ability to acquire new ideas from experience and to retain these ideas over time in memory. Moreover, unlike other mental processes such as thought, language, and consciousness, learning seemed from the outset to be readily accessible to cellular and molecular analysis. I, therefore, have been curious to know: What changes in the brain when we learn? And, once something is learned, how is that information retained in the brain? I have tried to address these questions through a reductionist approach that would allow me to investigate elementary forms of learning and memory at a cellular molecular level-as specific molecular activities within identified nerve cells.

/pdf/the-molecular-biology-of-memory-storage-a-dialogue-between-2cym9imp74.pdf

The Molecular Biology of Memory Storage: A Dialogue Between Genes and Synapses

Principles of neural science , Principles of neural science , کتابخانه دانشگاه علوم پزشکی و خدمات بهداشتی درمانی کرمان

Principles of Neural Science

Until recently, it has been impossible to approach learning with the techniques of cell biology. During the past several years, elementary forms of learning have been analyzed in higher invertebrates. Their nervous systems allow the experimental study of behavioral, neurophysiological, morphological, biochemical, and genetic components of the functional (plastic) changes underlying learning. In this review, we focus primarily on short-term sensitization of the gill and siphon reflex in the marine mollusk, Aplysia californica. Analyses of this form of learning provide direct evidence that protein phosphorylation dependent on cyclic adenosine monophosphate can modulate synaptic action. These studies also suggest how the molecular mechanisms for this short-term form of synaptic plasticity can be extended to explain both long-term memory and classical conditioning.

https://science.sciencemag.org/content/sci/218/4571/433.full.pdf

Molecular Biology of Learning: Modulation of Transmitter Release.

Biochemical and biophysical studies on Aplysia sensory neurons indicate that inhibitory responses to the molluscan peptide FMRFamide are mediated by lipoxygenase metabolites of arachidonic acid These compounds are a new class of second messengers in neurons

https://escholarship.org/content/qt848003wb/qt848003wb.pdf?t=ovgbfj

Lipoxygenase metabolites of arachidonic acid as second messengers for presynaptic inhibition of Aplysia sensory cells.

https://www.cell.com/cell/pdf/S0092-8674(02)01074-7.pdf

Integration of Long-Term-Memory-Related Synaptic Plasticity Involves Bidirectional Regulation of Gene Expression and Chromatin Structure

Cell Biology, Anatomy, and Development of the Nervous System. Signaling Within Nerve Cells. Signaling Between Nerve Cells. Cognitive Neural Science. Perception. Action. Genes, Emotions, and Instincts. Language, Learning and Memory

James H. Schwartz

Papers

Principles of Neural Science

Molecular Biology of Learning: Modulation of Transmitter Release.

Lipoxygenase metabolites of arachidonic acid as second messengers for presynaptic inhibition of Aplysia sensory cells.

Integration of Long-Term-Memory-Related Synaptic Plasticity Involves Bidirectional Regulation of Gene Expression and Chromatin Structure

Essentials of Neural Science and Behavior