Nucleuscoop Alpha 8 Download

I'm new to this program and I am quite confused. It seems like there is a lot of confusion in general. I see people asking how to use v10, and being given instructions that describe alpha 8 and give no help whatsoever with v10.

Hi!

I recently used alpha-tubulin to see if there was cytoplasmic contamination in my nuclear extracts and the corresponding band appeared. So there are two hypotheses: either my extracts are contaminated (can anyone suggest me a protocol to prepare nuclear extracts that guarantees no cytoplasmic contamination?) or alpha-tubulin is present in the nucleus. I'm hoping someone knows the answer. By the way, I use a monocytic cell line ( THP-1).

Thanks in advance

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I found an extraction protocol suggested by Sigma. It is not very different from the one I use by I'll try. I send it in attachment in case you want to take a look and give your opinions.

Back to alpha-tubulin, I would like to test it in a commercial nuclear extract sample to know, for sure, if this protein exists in nucleus. Do you know any company that sells this kind of product?

Thanks

Alpha-synuclein is a neuronal protein implicated genetically in Parkinson's disease. alpha-synuclein localizes to the nucleus and presynaptic nerve terminals. Here we show that alpha-synuclein mediates neurotoxicity in the nucleus. Targeting of alpha-synuclein to the nucleus promotes toxicity, whereas cytoplasmic sequestration is protective in both cell culture and transgenic Drosophila. Toxicity of alpha-synuclein can be rescued by administration of histone deacetylase inhibitors in both cell culture and transgenic flies. Alpha-synuclein binds directly to histones, reduces the level of acetylated histone H3 in cultured cells and inhibits acetylation in histone acetyltransferase assays. Alpha-synuclein mutations that cause familial Parkinson's disease, A30P and A53T, exhibit increased nuclear targeting in cell culture. These findings implicate nuclear alpha-synuclein in promoting nigrostriatal degeneration in Parkinson's disease and encourage exploration of histone deacetylase inhibitors as potential therapies for the disorder.

Nucleus pulposus (NP) cells of the intervertebral disc reside in an environment that has a limited vascular supply and generate energy through anaerobic glycolysis. The goal of the present study was to examine the expression and regulation of HIF-1alpha, a transcription factor that regulates oxidative metabolism in nucleus pulposus cells. Nucleus pulposus cells were isolated from rat, human, and sheep disc and maintained at either 21% or 2% oxygen for various time periods. Cells were also treated with desferrioxamine (Dfx), a compound that mimics the effects of hypoxia (Hx). Expression and function of HIF-1alpha were assessed by immunofluorescence microscopy, Western blot analysis, gel shift assays, and luciferase reporter assays. In normoxia (Nx), rat, sheep, and human nucleus pulposus cells consistently expressed the HIF-1alpha subunit. Unlike other skeletal cells, when maintained under low oxygen tension, the nucleus pulposus cells exhibited a minimal induction in HIF-1alpha protein levels. Electromobility shift assays confirmed the functional binding of normoxic HIF-1alpha protein to its putative DNA binding motif. A dual luciferase reporter assay showed increased HIF-1alpha transcriptional activity under hypoxia compared to normoxic level, although this induction was small when compared to HeLa and other cell types. These results indicate that normoxic stabilization of HIF-1alpha is a metabolic adaptation of nucleus pulposus cells to a unique oxygen-limited microenvironment. The study confirmed that HIF-1alpha can be used as a phenotypic marker of nucleus pulposus cells.

Strong evidence suggests a functional link between the melanocortin and dopamine systems. alpha-Melanocyte stimulating hormone (alpha-MSH) induced grooming behaviour, which can be blocked by dopamine receptor antagonists, is associated with increased dopaminergic transmission in the striatal regions. Whether this effect is mediated specifically by melanocortin (MC) receptors has not previously been established. Using in vivo microdialysis on anesthesized rats we have shown that alpha- MSH administered into the ventral tegmental area induced a significant increase in dopamine and DOPAC levels in the nucleus accumbens. This increase was completely blocked by pre-treatment with the MC4 receptor selective antagonist HS131, indicating that the effects of alpha-MSH on dopamine transmission may be mediated by the MC4 receptor.

In relaxed wakefulness, the EEG exhibits robust rhythms in the alpha band (8-13 Hz), which decelerate to theta (approximately 2-7 Hz) frequencies during early sleep. In animal models, these rhythms occur coherently with synchronized activity in the thalamus. However, the mechanisms of this thalamic activity are unknown. Here we show that, in slices of the lateral geniculate nucleus maintained in vitro, activation of the metabotropic glutamate receptor (mGluR) mGluR1a induces synchronized oscillations at alpha and theta frequencies that share similarities with thalamic alpha and theta rhythms recorded in vivo. These in vitro oscillations are driven by an unusual form of burst firing that is present in a subset of thalamocortical neurons and are synchronized by gap junctions. We propose that mGluR1a-induced oscillations are a potential mechanism whereby the thalamus promotes EEG alpha and theta rhythms in the intact brain.

Ac-225 is a high energy alpha-emitting radioisotope of increasing interest for clinical studies investigating the use of targeted radiopharmaceutical therapy, which combines select molecules with therapeutic radioisotopes to directly target and deliver therapeutic doses of radiation to destroy cancer cells in patients with serious disease. Ac-225 carries sufficient radiation to cause cell death in a localized area of targeted cells, while its half-life limits unwanted radioactivity in patients. Clinical research and commercial use of Ac-225 have been constrained by chronic short supply due to limitations of current production technology. NorthStar is positioned to be the first commercial-scale producer of n.c.a. Ac-225 and copper-67 (Cu-67) for advancing clinical research and commercial radiopharmaceutical therapy products. The Company will use its electron accelerator technology to produce n.c.a. Ac-225 that is free of long-lived radioactive contaminants and byproducts associated with other production methods. Such contaminants pose regulatory and waste management challenges for pharmaceutical companies, hospitals, and health systems.

Scientists soon learned that some of the mysterious rays emanating from radioactive substances were not rays at all, but tiny particles. Radioactive atoms emit three different kinds of radiation. One kind of radiation is a particle of matter, called the alpha particle. It has a positive electric charge and about four times the mass of a hydrogen atom. (We now know that it consists of two protons and two neutrons, the same as the nucleus of the helium atom.) Alpha particles exit radioactive atoms with high energies, but they lose this energy as they move though matter. An alpha particle can pass through a thin sheet of aluminum foil, but it is stopped by anything thicker. Beta rays, a second form of radiation, turned out to be electrons, very light particles with a negative electric charge. The beta particles travel at nearly the speed of light and can make their way through half a centimeter of aluminum. Gamma rays, a third type of radiation, are true rays, electromagnetic waves--the same kind of thing as radio waves and light, with no mass and no electrical charge. They are similar to, but more energetic than, the X-rays, an energetic form of electromagnetic radiation discovered by the German physicist Wilhelm Conrad Roentgen (1845-1923) in 1895. Gamma rays emitted by radioactive atoms can penetrate deeper into matter than alpha or beta particles. A small fraction of gamma rays can pass through even a meter of concrete.

O UNDERSTAND WHAT HAPPENS when radioactive atoms emit radiation, scientists had to understand how the atom is built. As Rutherford first explained in 1911, each atom is made of a small, massive nucleus, surrounded by a swarm of light electrons. It is from the nucleus that the radioactivity, the alpha or beta or gamma rays, shoot out. By around 1932 Rutherford's colleagues had found that the nucleus is built of smaller particles, the positively charged protons and the electrically neutral neutrons. A proton or a neutron each has about the mass of one hydrogen atom. All atoms of a given element have a given number of protons in their nuclei, called the atomic number. To balance this charge they have an equal number of electrons swarming around the nucleus. It is these shells of electrons that give the element its chemical properties.

When a radioactive nucleus gives off alpha or beta particles, it is in the process of changing into a different nucleus--a different element, or a different isotope of the same element. For example, radioactive thorium is formed when uranium-238--an isotope of uranium with 92 protons and 146 neutrons--emits an alpha particle. Since the alpha particle consists of two protons and two neutrons, when these are subtracted what is left is a nucleus with 90 protons and 144 neutrons. Thorium is the element of atomic number 90, and this isotope of thorium has an atomic mass of 234. The results of decay may themselves be unstable, as is the case with thorium-234. The chain of decays continues until a stable nucleus forms, in this case the element lead.

If IKK alpha localization in the nucleus is regulated by survivin-2B, it may be involved in regulating autophagy. Some groups have shown that nuclear IKK alpha is necessary for the stability of P73, a member of the P53 family that directly binds to the promoter of UVRAG and initiates its transcription. As expected, using an immunoprecipitation assay, we demonstrated that P73 interacted with IKK alpha in the nucleus of NB4 cells (Figure 4a). Meanwhile, we indirectly labeled IKK alpha and P73 with primary antibodies and observed obvious colocalization of IKK alpha and P73 in untreated NB4 cells, whereas this colocalization was canceled after selenite exposure (Figure 4b). As expected, the decrease of IKK alpha destabilized P73 and promoted apoptosis with increasing cleavages of caspase 9, caspase 3 and PARP, whereas downregulation of IKK alpha further inhibited autophagy by decreasing Beclin-1 and UVRAG (Figure 4d). Moreover, the CHIP assay explored that P73 could bind to the promoter of UVRAG, and this binding was attenuated after selenite exposure (Figure 4c). Similarly, the decrease of P73 expression could apparently promote selenite-induced apoptosis with enhancing cleavages of caspase 9, caspase 3 and PARP and further inhibited autophagy through the downregulation of Beclin-1 and UVRAG (Figure 4e). e24fc04721