I was recently asked to share my research at Umbrella Corp. I may also get to do a speaking gig at the Biotech Industry Growth Discussion and Intellectual Contribution Kvell.
My work in nerve regeneration and weaponizing
(being the best way to describe the planned process of repair) of certain DNA proteins
has been an important goal for the biotechnology dept. of Umbrella corp.
Three mechanisms of repair to the
double-strand breaks (DSBs) and flaying damage to axons is being worked on here
at Umberlla Corp. Two have been partially published in certain journals so
legally I have no trouble sharing some of this information with you.
Anon-homologous end joining (ANHEJ),
Using extracted Uracil-DNA
glycosylase from nematodes we are designing DNA-binding proteins that have a
specified DNA-binding site for regeneration, augmentation and enhancing of
spinal nerve endings as well as the cognitive brain functions of reposing test
subjects.
By placing single Zinc finger
protein to the severed end of certain flat worms we have been able to, through
said flat worm implantation, been able to create a "bridge" across
failed nerve endings. This along with specific gene protein protocols our group
has been able to bring positive response back from and into unresponsive (dead)
muscular tissue. Using this same process we have been able to generate certain
responsive activity in the cognitive brain areas of cadaverous test subjects.
Recently transcription
activator-like effector nucleases (TALENs) have been created, which are based
on natural proteins secreted by Xanthomonas bacteria via their type III
secretion system when they infect various plant species. These along with
specific growth gene proteins and gestation hormones from Neotomys ebriosus we
have been able to create some control over the test subjects.
To see if the nematodes can "automatically"
find and repair broken axons as they transverse through the host body the DOE
is to plant many of these modified nematodes into a test subject. While
"automatic" repair of mortified test subjects is evident, there is
still massive a loss of higher reasoning and fine motor control.
When the test subjects gain full mobility
they are single minded and focused on DNA extraction. It seems that for now the
instinctive memories and survival of the "bridge" symbiotes is to
obtain more DNA from subsisting sources for further repairs.
Micro-homology-Mediated End Joining
(MMEJ),
Using Trans-lesion synthesis (TLS)
as a DNA damage tolerance process we are allowing the DNA replication machinery
to replace past DNA lesions with thymine dimers to the axons AP sites. This
involves switching out regular DNA polymerases for specialized trans-lesion
polymerases (i.e. DNA polymerase IV or V, from the Y Polymerase family)
The ultimate goal being is the use
of bacterial cells and plasmids to replicate the same repair process of the
nematode but in a smaller vehicle. Progress here has been slow but there is
some positive direction, By controlling the formation of pyrimidine dimers with
irradiation from high wavelength UV light, the results in an abnormal covalent
bond between adjacent pyrimidine bases have shown to be receptive to photo-reactivation
process directly reversing the damage to the broken cells by the action of the
enzyme photolyase.
Another type of base excision
repair (BER) to the severed and or reposed nerve cells, which repairs damage to
a single DNA base pair caused by death is alkylation-hydrolysis which has shown
great promise in re-animation. The damaged base and glycosylase is removed by
the gestation androgynous hormone of a paddocstol and using phonosemantic
matching from inert Ebola DNA. The "missing tooth" is then recognized
by an enzyme called AP endonuclease, which cuts the phosphodiester bond. The
missing part is then resynthesized by a DNA polymerase where TALENs take
control of the growth, and the DNA ligase performs the final nick-sealing step.
Yes, the Nucleotide excision repair
(NER), is clumsy and not totally controllable, but with the Zinc finger protein
as a marker and extracted Uracil-DNA glycosylase in a synthetic reproduction environment
the bacteria in specialized synthetic polymerase plasmid envelopes should
recognize the bulky, helix-distorting lesions such as pyrimidine dimers and 6,4
photoproducts. With the specialized form of NER known as transcription-coupled
repair, the new self-replicating organism will deploy NER enzymes to genes that
are being actively transcribed.
Generation and control of self-replicating
and repairing, methylation of guanine bases, is directly accelerated by the
protein Methyl Guanine Methyl Transferase (MGMT), the bacterial equivalent of
which is called OGT. Right now this is an expensive process because each MGMT
molecule can be used only once. But we are also on the verge of being able to
force the MGMT to replicate itself using some of the DNA from the inert Ebola
virus DNA mentioned before.
The nerve cell and brain cell reaction
is stoichiometric rather than catalytic. And a generalized response to the methylation
agents in the bacteria are the adaptive response to and from the gestation androgynous
hormone of a paddocstol and confers a level of acceptance to alkylating agents
upon sustained exposure by upregulation of alkylation repair enzymes. The DNA
damage is reversed by neighboring cells as the repaired/replaced DNA is
certainly traded by methylation of the base pairs using the cytosine and
adenine found in the delivering plasmid envelope.
Homologous Recombination.
This, I am told cannot be talked
about without proper NDA filings and disclosure of asset investments to the
proper SEC channels
As you can see we are very busy at
Umbrella Corp and "We have your future in control."
Regards
John Sleestaxx
