CK2: Role In Memory And Learning

Mutations in this gene are responsible for an increased incidence of melanoma in a very small amount of families. The incidence of melanoma of CDK4 is similar to the families that have mutations in the gene CDKN2A. The gene CDK4 is a proto-oncogene that makes a protein that helps control cell division. However, when the CDK4 gene is mutated, it products an abnormal CDK4 protein that is too active. This abnormal protein makes cell divide uncontrollably fast, which could lead to tumor formation. Clinically, CDK4 and CDKN2A are mostly similar.

The limbic system (or Paleomammalian brain) is a set of brain structures including the hippocampus, amygdala, anterior thalamic nuclei, and limbic cortex, which support a variety of functions including emotion, behavior, long term memory, and olfaction.[1] The term "limbic" comes from Latin limbus, loosely translating as "border" or "belt".

Long-term potentiation refers to the steady increase in synaptic activity between two neurons which causes persistent strengthening of synaptic activity. Since memory formation is mainly dependent on synaptic strength, LTP seems to play an essential role in memory formation. Contrary to that, long-term depression causes a reduction in synaptic activity between two neurons, causing a decrease in synaptic activity. LTP and LTD are essential for normal functioning of the brain and balance in the ratio of LTP/LTD is needed for homeostasis. The levels and activity of LTP and LTD are majorly dependent on Calcium levels, Calcium-Calmodulin Kinase, NMDARs (N-Methyl-D-Aspartate receptors) and AMPARs (α-amino-3-hydroxy-5-methylisoxazole-4-propionic

Ketones and glucose are what feed the brain and keep it healthy and functioning properly. Ketones supply the brain with energy and when that happens it triggers the activation of proteins called brain derived neurotrophic factors (BDNFs). These BDNFs are what the brain uses for cell maintenance, brain repair and brain function.

The limbic system was first recognized due to Franz Josef Gall (LeDoux, J., 1996). Franz Joseph Gall developed the idea of “phrenology” that focused on the study of the different variations of bumps on the human skull to be related to differences in behavioral and emotional functioning. The limbic system’s main function in the brain is to control emotional behaviors and certain forms of memories that are infused with emotion (amygdala). The amygdala is a part of the brain that forms the tail end of the basal ganglia within the rostral temporal lobe and is located near the hippocampus (Lambert, K.G. & Kinsley, C .H., 2005). The amygdala, as defined by the text, is an almond-shaped structure that functions as a part of the limbic system involved in regulation of emotion and sexual urges (Lambert, K.G. & Kinsley, C .H., 2005). In addition, the amygdala is comprised of a dozen or more sub regions that are not all involved in fear conditioning (LeDoux, J., 1996).

(#2) CDKN1A is a protein coding gene. The purpose CDKN1A serves in the cell is that it works as cell cycle regulator at the G1 checkpoint and is responsible for the cell cycle arrest at that checkpoint. CDKN1A encodes a potential cyclin-dependent kinase (CDK) inhibitor which then prevents the phosphorylation of critical CDK substrates and blocks cell cycle progression, thus functioning as a cell cycle regulator at the G1 checkpoint. CDKN1A, along with p53, are both involved

At present, chemotherapy is the main systemic treatment option for TNBC patients. This study suggests a potential role for CDK7 in modulating the sensitivity of TNBC cells to the chemotherapeutic agent doxorubicin. This may provide additional therapeutic strategies for the fraction of TNBC patients with poor inherent response to doxorubicin, as well as those displaying residual disease following good initial response to treatment. A moderate level of increased sensitivity was also observed following CDK7 knockdown with carboplatin treatment, but not with docetaxel treatment, suggesting that the apparent protective effect mediated by CDK7 may be limited to genotoxic agents. Previous studies demonstrated that CDK7 played a positive role in DNA

Conducting specific aim one will focus on whether growth on collagen increases resistance to MEK. The extracellular matrix of these cells becomes dense with collagen, fibronectin, and proteoglycans and signaling from these components to the tumor cells through integrins contributes to drug resistance. Since collagen was present in large amounts in the poorly differentiated type, it is probable that collagen does affect tumor resistance to MEK inhibition. PTC cells with the MEK inhibitor were studied treated with collagen cells and untreated with collagen cells. Then, GR50 values were calculated so that normalized drug responses to growth rate were attained. When cell lines are plated, cell counts will be analyzed through a reagent that illuminates in the presence of ATP called CellTiterGlow. We will also evaluate phosphorylation within these cells to study how long inhibition occurs. Isolation of RNA will be isolated through Quiagen’s RNeasy isolation kit. We will use RT-PCR and Western Blotting to study MEK inhibition at the calculated GR50 and collect RNA from samples with and without collagen for transcriptome analyzation through RNA-seq. Sequencing libraries will be formed by using

Platelets are blood cells that, when activated aid in the clotting of damaged blood vessels; nevertheless, once these are compromised by cancer cells they contribute to the metastases of cancer. Cdk2 is a cyclin dependent kinase that is essential during the cell cycle due to its regulatory function. It is found to be inactive in in resting platelets; however, when the cell is stimulated with thrombin, Cdk2 has kinase activity. Although this enzyme is usually found in cell nuclei, the lack of a regulatory system in cancerous cells suggests that Cdk2 is no longer in the nucleus once the cell is compromised. Other parts essential in cell regulation signaling are the lipid rafts, also called microdomains, which are lipid and cholesterol-rich

Most research findings confirmed what prior research indicated – protein degradation and synthesis are essential in memory formation and memory formation relies on NMDA. However, the research indicated differences between the memory processes used by the hippocampus and amygdala in that prior researchers had found little evidence that protein degradation was a necessary part of the consolidation of memories in hippocampus. This led researchers to conclude that the amygdala and hippocampus may be more similar with regard to reconsolidation of memories than consolidation of memories.

IKBKB gene encoding the IkB kinase which plays an essential role in NFkB signalling pathway, it has kinase activity which phosphorylate the inhibitor of NFkB and targeting it for degradation, detail are shown as below.

The brain is dividing into several sections, including the cerebellum, the frontal lobe, and the temporal lobe, among others. The temporal lobe exists in two parts, one on each side of the brain close to the ears. It is largely responsible for the memory system (2). On the medial surface of the temporal lobe there are three important structure that are essential for human functioning. These structures are named, in order from rostral to caudal, the olfactory cortex, the amygdala, and the hippocampus. Together these three structures are referred to as the "limbic system" (1). Their functions became understood after studying how the brain functions upon loss of each structure. For example, in 1953, a patient suffering from epilepsy underwent surgery which removed most of his medial temporal lobe (1). After the surgery, the patient was able to remember who he was and was able to carry out coherent, intelligent conversations. However, if the person with whom he was talking left the room, he would have no

In recent years, a growing number of research has looked at the effects of stimulating brain oscillations on memory performance. Brain oscillations are fluctuations in local field potentials, caused by the input of neurons in to a specific cell assembly (Hanslmayr, Staudigl, & Fellner, 2012). In response to a stimulus, alpha (~10 Hz) and beta (~15-30 Hz) oscillation power decrease in activity, while theta (~4-7 Hz) and gamma (~40-100 Hz) oscillations increase (Hanslmayr & Staudigl, 2014). The changes in oscillatory power evoked by a stimulus modulate synaptic plasticity, the basis of memory formation (Düzel, Penny, & Burgess, 2010).

The authors took extracellular electrophysiological recording to examine the functional change from hippocampus on parabionts. They found isochronic parabionts stayed at baseline level for long-term potentiation, but can be maintained at above baseline level in heterochronic parabionts. From these functional results, they concluded that young blood is capable to potentiate synaptic plasticity in aged mice.