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Gia Voeltz (CU, HHMI) 2: Using BioID to Identify Membrane Contact Site Factors

October 21, 2019


6 Comments

  • Reply Robel Belay May 22, 2019 at 5:25 pm

    Great Lecture and a really cleverly designed identification scheme. Thanks for sharing!

  • Reply James Bogucheski May 22, 2019 at 6:51 pm

    Seems like antibody delivery is more effective on the late budding endosomes. Coronin 1C is a call function to the TMCC1 protein? Or was it illustrated to show the similarities with them?
    Either way, this might be the key to making more effective vaccines.

  • Reply Castello Jean May 23, 2019 at 4:09 am

    If electrons move through semiconductors the same way they do during a synapse would it be possible for an electron spin I guess if we was quantum we can just make our own biology yes, no ?

  • Reply José Antonio Fernández Robledo May 24, 2019 at 6:11 pm

    Great lecture!

  • Reply Juntao Yu July 8, 2019 at 12:34 am

    Nice advice on using BioID.

  • Reply Salvador Hirth October 16, 2019 at 10:34 am

    Professor Gia Voeltz, greetings from Brazil! I'll need to watch your entire lecture sometimes to absorb so much information. Your lecture is clearly the result of many years of research, thank you so much for sharing your knowledge! Do you believe that if CAG triplets could be transfected near palindromic regions of bacteriophages and then injected by said bacteriophages in the host bacteria, they could create a restriction enzyme capable of removing excessive CAG repeats that cause Huntington's disease? I am listening to your lecture hoping to learn more. I hope that it will be someday possible to get a special restriction enzyme through the nucleus membrane at will and direct such hypothetical enzyme to a target chromosome, during the S phase, to excise pairs of bases, maybe possible only in non methylated areas. I learned two days ago about how an error in an enzyme causes the methylation of of the 5 position on the pyrimidine ring of cytosines, creating 5-methylcytosine (5-mC); then, spontaneous deamination converts C in T; then I realized that it would create a STOP codon in two of the four possible codons for arginine and also in the codon CAG; the more cytosines, the more probable that a wrong methylation of a cytosine will occur, that would elucidate the mechanism that causes Huntington's and if the methylation is reversible at CG islands, it could even be part of the control of promoters. The funny thing is that I was looking for a way to produce stop codons at will as a way to hopefully stop protein synthesis in cancer cells and this mechanism already happens by accident and cause diseases.

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