ROMK2 (Miokatp) Channels: A Case Study

Understanding the activity of enzymes in different muscle types can aid greatly in obtaining more information about other processes such as metabolism of the tissues (Anderson et al., 2012). There are many different methods in order to achieve this information based in two different major categories but the most convenient method is one called continuous assay. This process includes the use of a spectrophotometer to continuously monitor the assay. This method allows for an easy way to calculate the initial rate of reaction as one can establish time points easily. In the lab performed the continuous method was used in order to determine the measurement of the activity enzyme succinate dehydrogenase (SDH). SDH is most commonly found in mitochondria. It is present in many different muscle tissues including the heart, red, and white tissue. In the following lab the enzyme was tested and measured in these three muscle types in the Oncorhynchus mykiss in order to determine which type contained the highest and the lowest activity. This enzyme is involved in multiple processes such as involved in both the Krebs cycle and the electron transport chain (ETC) (Smith, 2014). Its role in

The genes which encode for the mitochondria’s component proteins are in 2 separate genetic systems in 2 different locations. One of which is the cell nucleus, but the other is inside the organelle itself. There are relatively few genes inside the

The ATP-CP framework contains a collaboration between two particles, ATP and creatine phosphate (CP) inside the mitochondria of a cell. The CP atom discharges a lot of vitality when the bonds between its creatine and phosphate atoms are separated. This compound of creatine and phosphate (CP) is critical in this methodology. The ATP-CP pathway is the body 's essential quick wellspring of vitality of the three vitality frameworks. Exercises which oblige quick and prompt vitality are intensely reliant on this pathway. After ATP-CP is utilized up the other two vitality frameworks assume control.

I am conducting biomedical research in the laboratory of cardiac physiology under the mentorship of Dr. Elizabeth Murphy. Cardiovascular disease is the major cause of death in the US; therefore, a better understanding of the mechanisms regulating cardiomyocyte death in ischemia and reperfusion injury are important. Mitochondrial calcium plays a crucial role in the normal functioning of many processes, including the regulation of cardiac biochemical pathways and mediating ischemia-reperfusion injury. The uptake of calcium into the mitochondrial matrix is regulated by the mitochondrial calcium uniporter (MCU). An endogenous enzyme, Ca2+ Calmodulin Dependent Kinase II (CaMKII) has shown to regulate cell death and have increased activity during

Disorders in the mitochondria can cause a wide range of diseases. One of these is called mitochondrial myopathy. This word comes from myo, which means muscle, and pathos, which means disease. This disease causes prominent muscular problems. On patients with this disease we can usually find “ragged red”

ECSU. Succinate Dehydrogenase Activity in Isolated Mitochondria(2014): n. pag. Web.

Although significance was not reached, these results showed a trend for the abundance and localization of mitochondria/µm2 in RTT neurons to be higher than WT

C1.2.2. Optimization of analysis of movies of mitochondrial transport: In terms of acquiring the data for the large scale screen, we need to address important questions in terms of plate design and statistical analysis that build on our previous experience with such problems 18,44-47. In our initial studies described in C1.1.4, we assessed the effect of disrupting microtubules on mitochondrial transport by screening the plate before and after drug application. We did this because of the statistical power associated with paired measurements and because we were unsure how much well-to-well variation would impact the statistical analysis. Overall, we found that this provided an excellent means of measuring changes in mitochondrial transport. Having refined

The mitochondrial F1F0 ATP synthase is responsible for the ATP production in mammals via a rotary catalytic mechanism. Studies also show that the F1F0 ATP synthase can switch to an ATP hydrolase, which occurs under conditions during myocardial ischemia.

Figure 1. Dysbindin-1 controls mitochondrial length. Hippocampal slices cultured from sdy mice and their WT littermates were transduced with lentivirus expressing mitoDsRed (A–C), or cultured hippocampal neurons (WT) co-transfected with mitoDsRed and designated plasmids (D, E) were used for confocal imaging of mitochondria. (A) Representative images of mitochondria in the CA3 region; scale bar, 10 m. (B, C) Quantification for A; Mann-Whitney Rank Sum Test (B) and Student’s t-test (C) were used. (D) Representative images of transfected neurons; scale bar, 20 m for upper and 5 m for lower, enlarged images. (E) Quantification for D; one way ANOVA on ranks was used to compare across groups (H = 82.78, DF = 6, p < 0.001); Student’s t-test

Mitochondrial integrity is principal to efficient energy procedures and cardiac cell survival in response to diverse set of stressors, such as ischemia and various genotoxic parameters, such as infectious and immunological agents. The mitochondria are one of the major sources of adenine triphosphate, or ATP, via the electron transport chain/oxidative phosphorylation system and also provide a myriad service to the cell, such as pyruvate oxidation, the Krebs cycle, and amino acid, fatty acid, and steroid metabolism (3,4). The myocardium is a highly oxidative tissue, producing > 90% of its energy from mitochondrial respiration (5,6). However, at least 90% of the heart`s oxidative capacity is utilized during exercise, thus allowing for considerable

Three bands were distinguished (not including the standard curve bands), one band was present in the crude fraction lane and two bands in the mitochondrial fraction lane. No protein bands were present in the Nuclear fraction lane nor the soluble fraction lane. The Cox9 Ab binds to mitochondria so it was expected that the mitochondrial fraction lane would develop the most bands. Most of the mitochondria should be in the mitochondrial fraction. (Hart, 2017) The crude fraction lane also had mitochondria that interacted with Cox9 Ab, therefore, subcellular mitochondria was in the crude fraction, to a lesser extent. It was evaluated that the mitochondrial fraction proteins had greater migration (Table 9, 10, and 11) and density in comparison to the crude fraction lane. The ability to mark mitochondria with an Ab for further study is used frequently in scientific experimentation. (Edwards, Rawsthorne, & Mullineaux, 1990) Cell fractionation, SDS-PAGE, and Western blotting, is specifically used to study enzymatic activity. The mitochondria marked in the mitochondrial fraction lane could be collected for further purification and

To expand more on the relationship between mAChR’s, GTP- binding proteins, and the K+ channels, it is

This study has very specific measures and methods to acquire the best results to prove their hypothesis that, "the quantity of mitochondria present in prostate cancer cells might be of clinical relevance, and that the cellular mitochondria content might vary between prostate cancer subgroups harboring different key molecular alterations that might influence cell metabolism". First, prostate antigens levels were measured following patient surgery. The prostate specimens were embedded for histological analysis. Next, they took the a small core of tissue from each patient, the tissue was then distributed throughout 24 TMA blocks; each block containing the tumor samples. Lastly for the procedure each slide was exposed to heat and put into an autoclave before incubation with MTCO2. The study showed MTCO2 was within the cytoplasm of the prostate cancer cells and was intense compared to a normal prostate

This can be attributed to maximise efficiency and fidelity for oxidative phosphorylation. Increased fusion can also be seen when treatments which will directly or indirectly inhibit protein synthesis and by starvation and mTOR (mammalian target of rapamycin) inhibition–induced autophagy (10). Starvation-induced autophagy may increase the fusion rate by increasing dependence on oxidative phosphorylation via metabolism of lipids and proteins (9). Starvation may also bring about a specific stress response, Alternatively, starvation may mitochondrial hyperfusion (10), or it inhibit fission to protect mitochondria from autophagic catabolism (11). These effects are seen to aid mitochondrial dynamics maximise fidelity of oxidative phosphorylation on encountering