Using the ORegAnno Track in The UCSC Genome Browser to Research PIR' Regulatory Elements

This week I will continue to utilize the UCSC Genome Browser (http://genome.ucsc.edu) to investigate the PIR gene; particularly, I will be using the ORegAnno track within the database (Kent, Sugnet, Furey, et al., 2002). ORegAnno, short for Open Regulatory Annotation, seeks to document curated information concerning the regulatory factors of genes (Operators and operands, silencers, repressor proteins, transcription factors and cofactors, etc.). Previously in this blog I discussed the redox-sensitive nature of pirin, and how said redox-sensitivity may contribute to pirin acting as a transcriptional cofactor by allowing pirin to interact allosterically with transcription factors in redox-specific environments. Conversely, this week I will be focusing on the regulatory factors involved in the expression of the PIR (Pirin encoding) gene, rather than what regulations PIR expression may itself contribute towards. 

Navigating to the ORegAnno track for PIR on the Genome Browser returns several dozen regulatory elements for PIR. However, for the sake of my sanity and GPA amidst the ever encroaching finals week, I will only be listing the first three regulatory elements listed as examples of the types of data that the ORegAnno track provides users:

While I am not going into detail of all the regulatory elements for PIR provided by the  ORegAnno track, it is important to note that all of the elements listed are marked by orange indicators.  ORegAnno’s color coding dictates orange as representing transcription factor binding sites; thus the ORegAnno track relays the information that all of the regulatory elements for PIR that are listed in the ORegAnno database are transcription factor binding sites. When researching proteins, and by extension the genes that encode them, this type of data is invaluable. For instance, if a gene’s overexpression has been determined to be correlated to cancer progression, it is extremely beneficial to know under what conditions the gene downregulated and upregulated. 

Reflecting on the past assignments for this blog I still find the original summary of pirin that I wrote the most interesting project. Not only did such a dense topic outside of my field of study challenge me greatly, but it gave me the opportunity to educate myself on areas of biology far broader than pirin itself. For example, when my research showed me that pirin was a redox inhibitor for the NF-κB transcription factor, I had to educate myself on what redox reactions, protein complexes, transcription factors, allosteric reactions and far more biological concepts were to fully comprehend the information I came across. Moving forward, I would like to consider how the genes that the NF-κB transcription factor is responsible for are correlated to leukemia development, and thereby how pirin inhibition of NF-κB may also be correlated to the condition. A project along this line could utilize microarray assays to analyze gene expression in leukemic tissues. In addition, using the decentralization of pirin to detect melanoma via the staining techniques previously described in this blog would be a project that would allow me to familiarize myself with new (To me) lab techniques. I am also curious to further research the tissue specificity of pirin, as several of the databases and articles I have used in these past months have provided seemingly contradictory data in regards to pirin’s presence in myeloid cells, and by extension its potential role in hematopoietic maturation. 

References

Kent WJ, Sugnet CW, Furey TS, Roskin KM, Pringle TH, Zahler AM, Haussler D.  The
human genome browser at UCSC. Genome Res. 2002 Jun;12(6):996-1006.