Wiki Education Foundation-supported course assignment edit

  This article is or was the subject of a Wiki Education Foundation-supported course assignment. Further details are available on the course page. Student editor(s): Kbelardo.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 12:12, 17 January 2022 (UTC)Reply

Peer Edit edit

I really appreciate the content you added as it greatly contributed to the article. I felt like it was very readable and easy to understand given large amounts of technical information. I really appreciate the specific information regarding the structure and function of the protein and the protein images. Overall, it's a very solid article.

I would recommend elaborating on the relationship between VDAC1 and other diseases such as Parkinson's and Alzheimer's mentioned in the introduction. I know you described VDAC1's role in cancer and Amyloid β but I think expanding on this section would strongly tie together the rest of the article with the introduction. Nina.juansing (talk) 18:25, 22 November 2016 (UTC)Reply

EDITS edit

Peer review 1 Hi. I really think the edits you made contribute to the considerable bulk of the necessary material on this protein and I can better tell its function from your edits. Your specific edits on how VDAC1 acts as a calcium transporter is a major contributor to how it works in the body. I like the way you talked about how the fact that it can transport calcium affects certain parts of the TCA cycle or that it can trigger apoptotic reactions in a cell. It brought a random protein into the applicable world of science for the average biochem student. Additionally, speaking of the protein's function under certain separate voltage is key in understanding its regulatory cycles. I would have to recommend perhaps expanding on the light ideas you've added. I found that most information was peppered into each section and while that does have merit it doesn't seem like considerably substantial was talked about. Perhaps expand on the nature of the apoptotic mechanism or create more links to pages that can further expand on your ideas because I found myself asking more questions coming out than going into your edits. Also, expanding on what Amyloid Beta or linking it to a page would be useful. Itsimchi (talk) 09:19, 22 November 2016 (UTC)Reply

Hello, I was planning to add information pertaining to VDAC1 that was mostly obtained through research on murine VDAC1. This includes the following

  • add murine PDB (3EMN)
  • Add more visualizations of the pore from lateral views along with channel dimensions
  • Information on structure determination. i.e. discovered by 3 separate labs via x-ray crystallography (with citations)
  • Information debating the conformational mechanism of closure. i.e. N-terminus no longer shown to close the pore in mVDAC1 (with citations)
  • In the functions paragraph, I am going to add background on the outer mitochondrial membrane and the fact that it was once thought to be leaky but is now shown to be filled with VDAC1 channels that mediate flux of metabolites
  • Information on the voltage gating of the channel (under low voltage, it allows very little conductance whereas high voltage allows more conductance of ions)
  • More detailed information on how the MPTP complex forms along with visual representations

Please let me know if there are any comments questions of concerns. Kbelardo (talk) 01:41, 31 October 2016 (UTC)Reply

Found in pancreatic islet beta cells and possibly related to development of T2 diabetes edit

[1] also mentions VDAC2. A VDAC1 blocker has been patented as a treatment for diabetes. - Rod57 (talk) 14:02, 23 October 2018 (UTC)Reply