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202138//---1993，HTT，。，。
ScrippsSrinivasa Subramaniam，。 Subramaniam《Nature Communications》，。
（：Www.
pixabay.
com）
pixabay.
com）
Subramaniam：“，，。” “，，。。”，。 Subramaniam，。：“，。”
Subramaniam，。，。
，1010。DNA（CAG）。CAG，。HTT40，。，，，，。
，HTTCAG。Ribo-SeqCAG，mRNA-seq。
，，。，，。，Fmrp。
。，，。
Subramaniam，，。 “CAG，。CAG，，。”（ Bioon.
com）
：com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
com）
：com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
(Image source:style="text-align: justify;">Subramaniam said: "The ribosome must constantly move to build protein, but in Huntington's disease, the ribosome's efficiency slows down.
" "The difference may be two, three, or four times slower.
That's all the difference.
" Each cell is different.
Containing millions of ribosomes, they rotate together and use genetic information to assemble amino acids and make proteins.
Subramaniam said that impaired activity will eventually destroy the cell.
He said: "Without protein production, cells cannot survive.
"
" "The difference may be two, three, or four times slower.
That's all the difference.
" Each cell is different.
Containing millions of ribosomes, they rotate together and use genetic information to assemble amino acids and make proteins.
Subramaniam said that impaired activity will eventually destroy the cell.
He said: "Without protein production, cells cannot survive.
"
Subramaniam said that the latest developments in gene translation tracking technology made the team's discovery possible.
The results suggest a new treatment and have an impact on a variety of neurodegenerative diseases where ribosome stalls seem to play a role.
The results suggest a new treatment and have an impact on a variety of neurodegenerative diseases where ribosome stalls seem to play a role.
In the United States, Huntington's disease affects about 10 people per 100,000 people.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
In their experiments, the scientists used striatal cells designed to have three different levels of CAG repeats in the HTT gene.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
Scientists found that in Huntington's cells, the translation speed of many proteins slowed down.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
(Image source: style="text-align: justify;">Subramaniam said: "The ribosome must constantly move to build protein, but in Huntington's disease, the ribosome's efficiency slows down.
" "The difference may be two, three, or four times slower.
That's all the difference.
" Each cell is different.
Containing millions of ribosomes, they rotate together and use genetic information to assemble amino acids and make proteins.
Subramaniam said that impaired activity will eventually destroy the cell.
He said: "Without protein production, cells cannot survive.
"
" "The difference may be two, three, or four times slower.
That's all the difference.
" Each cell is different.
Containing millions of ribosomes, they rotate together and use genetic information to assemble amino acids and make proteins.
Subramaniam said that impaired activity will eventually destroy the cell.
He said: "Without protein production, cells cannot survive.
"
Subramaniam said that the latest developments in gene translation tracking technology made the team's discovery possible.
The results suggest a new treatment and have an impact on a variety of neurodegenerative diseases where ribosome stalls seem to play a role.
The results suggest a new treatment and have an impact on a variety of neurodegenerative diseases where ribosome stalls seem to play a role.
In the United States, Huntington's disease affects about 10 people per 100,000 people.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
In their experiments, the scientists used striatal cells designed to have three different levels of CAG repeats in the HTT gene.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
Scientists found that in Huntington's cells, the translation speed of many proteins slowed down.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Subramaniam said that the latest developments in gene translation tracking technology made the team's discovery possible.
The results suggest a new treatment and have an impact on a variety of neurodegenerative diseases where ribosome stalls seem to play a role.
The results suggest a new treatment and have an impact on a variety of neurodegenerative diseases where ribosome stalls seem to play a role.
In the United States, Huntington's disease affects about 10 people per 100,000 people.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
In their experiments, the scientists used striatal cells designed to have three different levels of CAG repeats in the HTT gene.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
Scientists found that in Huntington's cells, the translation speed of many proteins slowed down.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
In the United States, Huntington's disease affects about 10 people per 100,000 people.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
This is caused by too many gene repetitions of the three DNA building blocks (CAG).
The letters CAG stand for cytosine, adenine and guanine.
More than 40 of these repetitive sequences in the HTT gene can cause brain degenerative diseases and eventually lead to death.
The more repetitions, the earlier symptoms appear, including behavioral disorders, difficulty in movement and balance, weakness, and difficulty speaking and eating.
In their experiments, the scientists used striatal cells designed to have three different levels of CAG repeats in the HTT gene.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
Scientists found that in Huntington's cells, the translation speed of many proteins slowed down.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
In their experiments, the scientists used striatal cells designed to have three different levels of CAG repeats in the HTT gene.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
They used a technique called Ribo-Seq to evaluate the impact of CAG repeat sequences, and also used mRNA-seq to find out which genes are active.
Scientists found that in Huntington's cells, the translation speed of many proteins slowed down.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Scientists found that in Huntington's cells, the translation speed of many proteins slowed down.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
To confirm this finding, they blocked the ability of cells to make mutants of huntingtin and found that ribosome movement speed and protein synthesis increased.
They also evaluated how the huntingtin mutant protein affects the translation of other genes, and ruled out the possibility that another ribosome binding protein, Fmrp, might cause a slowing effect.
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Further experiments provide some clues for how mutant huntingtin interferes with the work of ribosomes.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
They found that it directly combined with ribosomal protein and ribosome assembly, not only affects the speed of protein synthesis, but also affects the density of the cell's ribosome.
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Subramaniam said that there are still many problems, but this progress provides a new direction for helping Huntington's disease patients.
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
"The idea that the ribosome can stall before CAG repeats is what people had expected, and we proved it does exist for the first time.
To figure out how CAG repeats slow down the ribosome, a lot of extra work is needed, and then maybe We can develop drugs to counteract this effect.
" (Bioon.
com)
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Information source: com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Information source:
com/news/2021-03-huntington-disease-driven-protein-building-machinery.
html">Huntington's disease driven by slowed protein-building machinery in cells
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
DOI: 10.
1038/s41467-021-21637-y
Original source: Mehdi Eshraghi et al, Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature Communications (2021).
DOI: 10.
1038/s41467-021-21637-y
Original source: Mutant Huntingtin stalls ribosomes and represses protein synthesis in a cellular model of Huntington disease, Nature CommunicationsDOI: 10.
1038/s41467-021-21637-y
