There are some other things in genetic-modifications.csv.
Gene candidates for germline genetic modification
Direct gene candidates
There are a number of options here, but with germline modification, a muscle-specific knockout of ACVR2B or myostatin are good choices. Also follistatin overexpression in muscle.
In muscle, this allows greatly improved metabolism and endurance (see 'mighty mice'). Synergistic effect with myostatin inhibition is untested, but intriguing.
As the "guardian of the genome", p53 is missing in many cancers, and has been investigated as a gene therapy option for cancer. Introducing a separate copy, or copies of the gene from the wild-type could reduce the incidence of knockout mutations that normally lead to cancer.
Humans are unsuited to digesting some types of branching carbohydrates, which then pass through the intestines and feed annoying bacteria. Not a huge priority, but with the increased metabolic demands from the muscle-enhancing therapies, it can't hurt.
Provides resistance to HIV and plague. Increases risk from West Nile virus, but who gives a fuck about that.
Also see HCP5 (rs2395029), and CCL3L1.
LRP5 gene (strong bones)
Those with the LRP5 gene have extra strong bones.
PCSK5 (lower coronary disease)
Those with the PCSK5 gene have 88 percent lower coronary disease.
FUT2 (norovirus / stomach flu resistance)
Those with double FUT2 are resistant to stomach flu.
Lactase persistence (lactose tolerance)
Also known as "C/T(-13910)", and located in the MCM6 gene but with influence on the lactase LCT gene, rs4988235 is one of two SNPs that is associated with the primary haplotype associated with hypolactasia, more commonly known as lactose intolerance in European Caucasian populations. [PMID 11788828], [PMID 15114531]
In these populations, the rs4988235(T) allele is both the more common allele and the one associated with lactase persistence; individuals who are rs4988235(C;C) are likely to be lactose intolerant. In populations of sub-Saharan Africans, though, the rs4988235(T) allele is so rare that it's unlikely to be predictive of lactase persistence, and other SNPs are predictive instead. [PMID 15106124, PMID 17159977]
Hyperosmia (increased odor sensitivity)
rs1953558 - sensitivity to sweaty odor (isovaleric acid)
DARC - rs2814778
HBB - i3003137
G6PD - rs1050828
sweetness - TAS1R2
umami - TAS1R1
sourness - PKD2L1
spiciness - TRPV1
signal - GNAT3, TRPM5, PLCB2
bitterness - TAS2R4, TAS2R5, TAS2R16, TAS2R8, TAS2R38, TAS2R48
Sprinting vs. endurance
ACTN3 - rs1815739
Theoretical "heterozygote advantages" genes
The principle here is that diseases such as sickle cell or Tay-Sachs, among many others, persist in a population because having one 'good' and one 'bad' copy of the gene offers a significant advantage - in disease resistance, intelligence, etc.
While it would be nice to find a point mutation that would mimic the benefits of heterozygosity, the most straightforward option would be to give someone both variants of the gene, with ~50% expression of each.
Tetracycline response elements, i.e. tet-on and tet-off, can be used for transgenes where constant expression is undesirable. While a number of options for such inducible expression exist, the tet system is the most studied. It is left as an exercise to the reader to determine which genes would be suitable candidates [I will add some when I get around to it].
Candidate genes for sports doping
This is lifted from this table.
|Gene/product||System/organ targets||Gene product properties||Physiologic response|
|ACE||skeletal muscles||peptidyl dipeptidase||ACE-D is involved in fast twitch muscles.|
|ACTN3||skeletal muscles||actin-binding proteins related to dystrophin||Involved in fast-twitch muscles.|
|endorphins||central and peripheral nervous system||widely active peptides||pain modulation|
|EPO||hematopoietic system||glycoprotein hormone||Increases RBC mass and oxygen delivery.|
|HGH||endocrine system||191-amino acid protein||Increases muscle size, power, and recovery.|
|HIF||hematologic and immune systems||multisubunit protein||Regulates transcription at hypoxia response elements.|
|IGF-1||endocrine/metabolic/skeletal muscle||70-amino acid protein||Increases muscle size, power, and recovery by increasing regulator cells.|
|myostatin||skeletal muscle||2-subunit protein||Regulates skeletal muscle. Inhibition increases muscle size, power, and recovery.|
|PPAR-delta||skeletal muscle and adipose tissue||nuclear hormone receptor protein||Promotes fat metabolism and increases number of slow twitch fibers.|
|VEGF||vascular endothelium||glyosylated disulfide-bonded homodimers||Induces development of new blood vessels.|
Abbreviations: ACE, angiotensin-converting enzyme; ACTN3, actinin binding protein 3; EPO, erythropoetin; HGH, human growth factor; HIF, hypoxia inducible factor; IGF-1, insulin-like growth factor; PPAR-delta, peroxisome proliferators-activated receptor (delta); VEGF, vascular endothelial growth factor.
Originally authored by yashgaroth on 2012-06-28. See http://gnusha.org/logs/2012-06-28.log for more context.