This research studies about the unique role of HAUSP in the p53-Mdm2 pathway. p53 is a tumor suppressor gene, so not only does it stop the formation of tumors but can also arrest growth and initiate apoptosis. Stabilization of p53 is important for these functions to occur. Now ubiquitination of proteins is useful in many cellular processes and Mdm2 mediates p53's degradation. Mdm2 is an oncoprotein that binds and blocks the N terminus of p53 repressing its activity, but interestingly p53 activates the transcription of Mdm2.
In its controversial discovery, the p53 protein was first identified as an oncogene because of its association with the simian virus 40 (SV40) large T-antigen (Lane and Crawford 1979; Linzer and Levine 1979). Subsequently, it was observed that many tumors express this protein in excess quantities, suggesting once more that p53 might act as a cellular oncogene (DeLeo et al. 1979; Rotter 1983). This notion was reinforced when investigators, Eliyahu et al. and Parada et al., ectopically expressed the newly cloned p53 cDNAs into primary cells.
Apoptosis is a form of cell death which is an essential process for growth and development of multi cellular organism and removes damaged cells to prevent inflammation (Madeo, Frohlich et al. 1997). In addition, apoptosis can be morphologically characterized by cell shrinkage, chromatin condensation, and formation of apoptotic complex (Madeo, Frohlich et al. 1997,Qi, Kim, et al. 2013).The main biochemical characteristics of apoptosis include caspase activation and DNA fragmentation (Madeo, Frohlich et al.
et al have demonstrated that, together, TLR7 and TLR9 likely form a functional subgroup within the TLR family that recognize pathogen-associated molecular pattern (PAMPS) in endosomal compartment. It is now clear TLR7 and TLR9 play a significant role in the recognition of vesicular stomatitis virus and CpG bacteria DNA, thereby activating the innate immune system. The experiments with TLR7 and TLR9 deficient mice have shown the essential role in the recognition of ssRNA by TLR7 and non-methylated CpG bacteria DNA by TLR9 respectively.
As a result these factors stimulate interferons and other cytokines in innate immunity. Method Many steps were ... ... middle of paper ... ...onse to occur. Further research was done to see if HIV infection produces retroviral cDNA in the cytoplasm, if cGAS was activated when infected with HEK293T cells with HIV-GFP. In the cytosol purified cGAS proteins were prepared for ATP and GTP. The results show that cytosolic extracts from HIV infected cells did stimulate cGAS.
This will be interpreted as a specific endonuclease being recruited by the Cas9-tracrRNA-scaRNA-mRNA complex for degradation. Limitations: Some of these nucleases may have degenerate functionality. Failing to find increased FTN_1103 halflife, deletion combinations of these six endonucleases will be created and tested similarly. It is also possible that the endonuclease required is undescribed or otherwise not tested. If the deletion assays fail, protein crosslinking in vivo during phagosome infection will be performed in cells expressing myc-tagged Cas9.
link this unique MHC gene organization to the structure of the MHC by showing that MHCI molecules have novel combinations of signal sequences which possibly led to MHCII like function. Using spleen tissue they generated cDNA through the use of PCR reactions in order to complete coding region of MHCI. They then examined the binding pocket component encoded by this data and were able to identify several conserved structural and functional sequence... ... middle of paper ... ...n the past. Evolution such as this helps to battle the every changing pathogens. References 1.
To investigate the effect of aforementioned fusion peptides, pIRES/mda-7, pIRES/mda-7-RGD1 and pIRES/mda-7-RGD2 constructs werre prepared during some cloning steps. The expression of related proteins evaluated via RT-PCR and IF assays. It was shown that our modified mda-7 proteins were expressed in considerable rate in HEK293 and Huh-7 cell lines. Therefore, the results suggested that these constructs are able to be employed for future researches. In our knowledge publications that token the advantage of RGD peptide for improving the specificity and efficacy of mda-7 in gene based therapy is limiting (20).
Yeast cells, or Saccharomyces cerevisiae, that had mutated transport mechanisms established a genetic basis for vesicle transport and fusion to the plasma membrane. From these cells, it is possible to isolate regulatory genes that encoded proteins essential to intracellular transport. Kaiser and Schekman (1990) specifically analyzed the SEC proteins: manipulation by mutation reveals that construction of vesicles is dependent on SEC prot... ... middle of paper ... ...abetes, which occurs from failure in insulin secretion and glucose transport. Immunological reactions are also dependent on vesicle transport because they must have a mechanism to release cytokines in response to threats. Additionally, medical relevance stems from the effects of mutations on genes that encode proteins responsible for vesicle transportation.
One of the research interests involves the development of novel treatments against the multi-drug resistant property of ABC transporters in treating relevant human diseases such as cystic fibrosis and Tangier disease (Stefková et al., 2004). With any of such novel applications, a substantial knowledge on sequence motifs in terms of their functional significance is required. In this essay, the discussion is limited to protein sequence signatures in nucleotide binding domains (NBDs) of ABC transporters relating to substrate translocation. It will be seen that the protein sequence motifs perform similar function across species, and any mutation can affect its overall function. However, it should also be noted that these motifs can result in slightly different mechanism in different species, and that they can perform their function at certain domains of the protein.