C-JUN
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C-JUN
C-jun is a protein which has evolved over a long period of time and it has effects both on the human body as well as other parts of the body. it in the human body this virus is coded using the JUN gene. In combination with the c-Fos, this virus forms early response transcription factor known as AP-1. Fistly this protein was discovered as Fos-binding protein f 39 however with time it came to be discovered as related to JUN gene and as its product. For the proto-oncogen which is c-jun, it I the cellular homolog of v-jun. the human protein and the viral protein are similar and therefore encoded almost in a similar manner. Discovered in avian sarcoma virus seventeen, the viral homolog v-jun was named as ju-nana. Ju-nana is the Japanese word for number seventeen and therefore this is an indication of the geographical location in which it was discovered. The human jun encodes with a protein that is in close interaction with specific dna sequences. This type of interaction is for the sake of controlling gene-expression. Being intronlesss, the gene is mapped onto a region involved in both deletions in humans and translocations.
A protein has to perform its functions and it is for these functions that proteins are synthesized on demand as the need arises for them to be used in a particular function within the body. The DNA contains the correct protein encoding information for any protein. Nucleosomes are composition of chromosome structure basic units and they are a representative form of high structure of DNA. Jun and its partners in ap-1 are highly subject to regulation by multiple extra-cellular stimuli. The activation of transcription machinery requires a release of a DNA compaction and the histone post modulational translations. For RNA transcription one strand of DNA is used and the RNA produced is complementary to the dna strand which is complimentary (5Xia, et,al, 2013)
The jun protein is composed of three members. These members include; c-jun, junB and junD . the three members are disctinct and sometimes play roles which can be termed as antagonistic. C-jun is the oldest member of this protein family. junB and junC share about 45% of amino acids but still they are in different in their structure and function. One of the differences is that junB contains a JNK docking domain for acids 35 and 61 while on the other junC this does not exist. Therefore this is an indication that the activation of junB is independent of JNK activation. In junC phosphorylation Trans-activates the protein while phosphorylation in junB leads to its degradation. Sumoylation in T cells reduces the activity of junB as well as the subsequent cellular activation. junB does not form homodimers as spontaneously as junc does. These differences also include those of the mode of gene regulation and signalling pathway activation.
junD is a transcription factor that is encoded by jund gene in humans. It is one of the members of jun family as well as a functional component of complex transcription factor ap1. The negative mutant variant which is dominant acts as an antagonist transcript. It opposes many neurological changes that occur specifically with addiction.
The G1 phase of cell cycle requires c-jun for its progression. Increased G1 arrest is shown by c-jun null cells. C-jun is actively incloved in the regulation of the transcriptional level of Cyclin d1, which is a major rb kinase. Rb kinase is a growth suppressor which is inactivated by phosphorylation. It is therefore true that the presence of cjun is important in maintaining sufficient d1 kinase activity. When c-jun is absent cells show a cell cycle defect.
There have been many researches about cjun and focusing on its different components which have resulted into different kinds of results and information. Therefore focusing on two of these researches ill discuss about the findings and what the role of cjun isin these researches. In the research published by Sehwan Jang, Li-Rong Yu, Mohamed A. Abdelmegeed, Yuan Gao, Atrayee Banerjee and Byoung-Joon Song, the very essential and important role of c-jun N-terminal protein by the name of kinase in promoting mitochondria dysfunction and acute liver injury is discussed. In their research they used rats to test for the mitochondria dysfunction and acute liver injury when cjun N-terminal was used. They thus needed to portray and display in a better manner and to provide an understanding to many people on how n-terminal kinase promotes tissue injury, a concept which is rarely understood by many people.
The use of rats was also an essential part of the research as rats are easy to study. Therefore young male mice were exposed to a single dose of CCL4 and were euthanized at different points. Some of the major measurements included blood alanine aminotransferase, liver histology and other enzyme activities were also measured. With this kind of experiment the liver damage was maximal at 24 hours after the first injection. This research was also inspired by the fact that most of the people suffer from acute liver failure which is caused by overdose of potentially toxic components like acetaminophen, binge alcohol and cocaine. In the United States more than 56000 room visits were due to APAP induced acute liver injury and out of these there are about 400 deaths. Therefore there was a need to investigate into the issue of liver problems associated with apap and the deaths thus the research (Jang et,al, 2015)
The research therefore found out that alcohol and other components consumed have these components which make it easy for liver destruction while at the same time it is possible to have cell damage leading to more complications and even death in some cases. Even though these components are mild they serve a prolonged time before the effects can be seen and thus makes a person’s life in danger because the liver is always one of the most complex parts of the human body to treat and make sure the infection does not re-occur. Therefore even though some drugs like APAP are allowed and regulated by FDA they still have an effect and impact on the human health and can cause complications. The complications arise especially when these drugs are not used in the right manner and when they are misused.
Another research which has been carried out in related to c-jun protein is the research about the role played by differential regulation of c-jun proteins in chemoresistance of cancer cells. cisplatin is a drug used mainly for chemotherapy and it has had issues to do with what leads to its resistance by the tumors and this has been alarming. Therefore in this concern Yan Xia, Weiwei Yang, Wen Bu, Haitao Ji, Xueqiang Zhao, Yanhua Zheng, Xin Lin, Yi Li, and Zhimin Lu carried out a research into this issue to determine how the regulation of cjun could be of effect in minimising or increasing the acceptability of the medication by the body of a person infected with cancer. In the research the treatment with cisplatin which can also be abbreviated by CDDP resulted into downregulation of C-jun expression. There was also observance and finding of the degradation of c-jun in cancer-sensitive cells. Expression of cleavage resistant mutant supressed CDDP induced aspoptotis of sensitive cells. These findings therefore suggest that c-jun is a perfect target for the improvement of cancer therapy (Marques et.al, 2014).
These two researches play a big role when it comes to c-jun and its relation to other aspects of the human body and how these affect the process and the issue of functionality and ability to be properly organised. Therefore it is of essence to know what it means to study c-Jun and also what this specific protein means for the other proteins, how they react, the vulnerabilities of this protein as well as its stregths which can be used to provide better medication and other solutions to the human problems.
It is indeed true that this is a protein which belongs to a higher group of the gene of Jun thus it has so many relations within the human body. From the above researches we can also identify it is not only found in humans but also found in many other animals like the rat which was used for experiment in the first research discussed and summarised. This makes it even easier and better for the researchers to be able to research more keenly and with confidence the different aspects of this proteins and how they affect the human body from different angles and aspects using different animals.
References
Marques, N., Sesé, M., Cánovas, V., Valente, F., Bermudo, R., De Torres, I., … & Paciucci, R. (2014). Regulation of protein translation and c-Jun expression by prostate tumor overexpressed 1. Oncogene, 33(9), 1124-1134.
Xia, Y., Yang, W., Bu, W., Ji, H., Zhao, X., Zheng, Y., … & Lu, Z. (2013). Differential regulation of c-Jun protein plays an instrumental role in chemoresistance of cancer cells. Journal of Biological Chemistry, 288(27), 19321-19329.
Mialon, A. (2009). Role and function of c-Jun pRotein complex in canceR cell behavioR.
Jang, S., Yu, L. R., Abdelmegeed, M. A., Gao, Y., Banerjee, A., & Song, B. J. (2015). Critical role of c-jun N-terminal protein kinase in promoting mitochondrial dysfunction and acute liver injury. Redox biology, 6, 5Xia, Y., Yang, W., Bu, W., Ji, H., Zhao, X., Zheng, Y., … & Lu, Z. (2013). Differential regulation of c-Jun protein plays an instrumental role in chemoresistance of cancer cells. Journal of Biological Chemistry, 288(27), 19321-19329.52-564.
