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Sasicha Manupipatpong

Gene switches do more than flip 'on' or 'off': Can exhibit much more complex binding be... - 1 views

  • right genes for the job are turned on only in the specific cells where they are needed
  • molecular "clutch" that converts treadmilling to a stable bound state, moving the transcription process forward to completion to turn the gene on
  • act like a switch; they are either "on" (bound to DNA) or "off" (not bound)
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  • can exhibit much more complex binding behavior
  • transcription factors' binding process is dynamic and involves more than just being bound or unbound
  • In addition to a stable binding state (on or off)
  • "treadmilling," where no forward transcription process is occurring
  • indicator of whether a gene was turned on or off
  • measure and calculate how long a protein is associated with all of the different genes it regulates
  • proteins that bind in the stable state are associated with high levels of gene transcription
  • if we can regulate the transition between treadmilling and stable binding, we can regulate the outcome in terms of gene expression
  • genetic medicine -- a new way to regulate the 'switches' that turn gene expression associated with disease on or off.
  • measured how long it took the competitor transcription factor to replace the resident protein and used this data to calculate the residence time at each location in the genome
  • specific proteins called "transcription factors" that control which genes are turned on or off in cells by binding to nearby DNA
  • new insights on how cells respond to developmental cues and how they adapt to changing environmental conditions
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    Genes have been discovered to be more complex than we previously thought--rather than having only on and off states, there is an intermediate state called "treadmilling".
nidthamsirisup

Engineered stem cells seek out and kill HIV in living mice - 0 views

  • human stem cells can be genetically engineered into HIV-fighting cells
  • surrogate model
  • CD8 cytotoxic T lymphocytes -- the "killer" T cells that help fight infection -- from an HIV-infected individual and identified the molecule known as the T cell receptor, which guides the T cell in recognizing and killing HIV-infected cells.
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  • cloned the receptor and used this to genetically engineer human blood stem cells.
  • mature T cells that can attack HIV in tissues where the virus resides and replicates.
  • CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections.
  • CD4 "helper" T cells
  • engineering stem cells to form immune cells that target HIV is effective in suppressing the virus in living tissues in an animal model
  • increased
  • HIV in the blood decreased.
    • wasin kusakabe
       
      Using mice as lab rats, researchers are able to produce a large amount of T cells that can fight off HIV more effectively.
  • The engineered stem cells developed into a large population of mature, multi-functional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also discovered that HIV-specific T cell receptors have to be matched to an individual in much the same way an organ is matched to a transplant patient.
  • Expanding on previous research providing proof-of-principle that human stem cells can be genetically engineered into HIV-fighting cells
  • In this current study, the researchers similarly engineered human blood stem cells and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates. They did so by using a surrogate model, the humanized mouse, in which HIV infection closely resembles the disease and its progression in humans.
  • increased, while levels of HIV in the blood decreased. CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections. These results indicated that the engineered cells were capable of developing and migrating to the organs to fight infection there.
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    Stem cells that are engineered to produce T cells that can help fight off HIV.
Nitchakan Chaiprukmalakan

Missing Lincs - Science News - 6 views

    • Nitchakan Chaiprukmalakan
       
      Scientists are finding more information about the importance of the non coding RNAs, lincRNAs.
  • Only now have scientists begun identifying the previously invisible contractors who make sure that materials get where they are supposed to be and in the right order to build a human being or any other creature. Some of these little-known workers belong to a class of molecules called long intergenic noncoding RNAs.
  • And the lincRNAs originate in what scientists used to view as barren wastelands between protein-coding genes. But new research is showing that these formerly underappreciated workers have important roles in projects both large and microscopic.
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  • In the last few years, scientists have learned that lincRNAs, as well as other RNAs that are long and noncoding but not intergenic, perform a variety of jobs. Some serve as guides showing proteins where to go, while others tether proteins to different types of RNA, or to DNA. Some work as decoys, distracting regulatory molecules from their usual assignments. Some may even have multiple roles, all the while chattering away to other RNA within cells. (It is not idle gossip; RNA communication within cells may ward off diseases such as cancer.) And as the ultimate multitaskers, lincRNAs keep proper cellular development ticking along and help define what makes mice mice and people people.
  • That archive contains about 3 billion genetic letters, far more than the genomes of less complex organisms such as roundworms and fruit flies.
  • In 2005, the research revealed that even though genes that code for proteins make up only 1.5 percent of the mouse genome, more than 63 percent of the genome’s DNA is copied into RNA. In humans the number is even higher, with up to 93 percent of the genome made into RNA, even though protein-coding genes make up less than 2 percent of the genome.
  • At first, many scientists didn’t know what to make of the excess RNA. Some thought it was overexuberance on the part of the DNA-copying machinery. But gradually researchers began to realize that many of those extra RNAs had important jobs to do.
  • Some, though, appear to act like general contractors — not hammering in the nails and pouring the foundations of cells themselves, but dictating how the job should be done.
  • One of the most famous long noncoding RNAs, known as XIST, is also one of the most hands-on. XIST is in charge of shutting down one of the X chromosomes in every single cell of women and girls
  • XIST doesn’t have a long commute to work; it coats whichever X chromosome makes it, preventing other genes on the chromosome from being activated
  • One of the most well-studied linc­RNAs, named HOTAIR, wasn’t lucky enough to get a job close to home. It is copied from DNA on chromosome 12 but has to travel to chromosome 2 to shut down several genes in a group known as the HOXD cluster, genes important for proper development of an organism
  • Not only does HOTAIR help direct development, but it is also important throughout life to help cells pinpoint their location in the body.
  • Whether promoting health or mis­directing cells, lincRNAs don’t necessarily act alone.
  • A lincRNA known as HOTTIP also works with a crew of histone modifiers, but instead of shuttering genes, HOTTIP’s crews hang grand-opening signs to attract gene-activating machinery
  • In the recipe for humans, lincRNAs are in the thick of things from the very beginning. At least 26 different lincRNAs need to be on to keep an embryonic stem cell a stem cell
  • Just how lincRNAs choose which genes to turn on and off isn’t yet known. But Pier Paolo Pandolfi, a geneticist at Beth Israel Deaconess and Harvard Medical School, suspects that the lincRNAs are whispering to each other and to other RNAs, keeping tabs on all a cell’s goings-on. Pandolfi laid out his hypothesis for how this chatter might help control protein production and other processes in the Aug. 5 Cell.
  • The Columbia team and Pandolfi’s team independently found that tweaking levels of a few messenger RNAs that distract microRNAs from PTEN messenger RNA can lead to prostate cancer or a type of brain tumor called glioblastoma. Just messing with levels of a messenger RNA from another gene known as ZEB2 throws off PTEN protein levels and can lead to melanoma in mice, Pandolfi’s group reported in another paper in the Oct. 14 Cell.
  • Losing one noncoding RNA may be disastrous for a cell, but for want of noncoding RNAs whole species may never have evolved, argues Queensland’s Mattick. He and others say the real function of lincRNAs is to give evolution a sort of molecular clay from which to mold new designs.
  • Humans have several lincRNAs that are found in no other species. Many of those RNAs are made in the brain, leading scientists to speculate that the molecules may be at least partially responsible for that important organ’s evolution.
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    Is RNA the most important molecule in the cell? There is a lot of evidence leading to new understandings of RNA and it's role in many different mechanisms within a cell.
Mickey Tsai

Niceness a combination of genetics and environment, the Neurogenics of Niceness study f... - 0 views

  • BEING a nice person could come down to having a good set of genes
  • "kind" behaviour of more than 700 individuals was partly linked to receptor genes for oxytocin and vasopressin.
  • uch of the hormone you have, it's how responsive your brain is to the hormo
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  • It's not about how much of the hormone you have, it's how responsive your brain is to the hormones
  • "(Niceness) is a combination of genetics and your environment."
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    A study shows that genetics could play a role in determining "niceness". The kind behavior is found to be linked to receptor genes for oxytopic and vasopressin. People that are more responsive to it are more inclined to donate money, pay taxes, give blood, report crime etc. It isn't about how much of the hormone you have but how responsive you are to it. Of course genetics isnt the only factor, if you are surrounded by nice people it is likely that it would rub off on you.
Sea Maskulrath

Scientists clone pashmina goat - Hindustan Times - 0 views

  • three years of producing the first-ever buffalo animal clone, Indian scientists have now successfully cloned the world's first pashmi
  • The cloned baby is kept under medical observation at the off campus sheep breeding centre and is in "fine health"
  • The cloned was produced with the help of a cost-effective "hand guided t
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  • echnique" and NDRI had used the same technology to clone two buffalo calves on its Karnal campus.
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    Now that the cost of the pashmina will be lowered, we have to thank Dr.Tej for his hard work and that we cannot underestimate indian biotechnology.   
Mickey Tsai

Autism gender bias clue found - Health - CBC News - 0 views

  • four times more common among males than females.
  • rare family with four generations in which males carrying the glitch were affected but females were not.
  • When male fetuses are missing one copy of the gene, it throws off their developmental process enough to lead to autism but female biology differs enough that it doesn't matter.
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  • now that doctors know that the SHANK 1 gene is involved and it can be tested for, they'll know to follow affected males very closely and offer treatments early on.
  • lved and it can be tested for, they'll know to follow affected males very c
  •  
    Scientists have long wondered why autism is much more common among males than females. When males miss one copy of a gene it messes up the development process enough to cause autism but female biology differs enough to make it not matter. Now that scientists have identified that the SHANK 1 gene is involved they can test for it and could offer treatments early.
nidthamsirisup

Mysterious Noncoding DNA: 'Junk' or Genetic Power Player? | PBS NewsHour - 0 views

  • Genes represent only a tiny fraction -- 1 percent -- of our overall genetic material. Then there's the other 99 percent of our DNA -- the stuff that doesn't make protein
  • Researchers have found that some of this noncoding DNA is in fact essential to how our genes function and plays a role in how we look, how we act and the diseases that afflict us.
  • Embedded in this 99 percent is DNA responsible for the mechanics of gene behavior: regulatory DNA. Greg Wray of Duke University's Institute for Genome Sciences and Policy describes the regulatory DNA as the software for our genes, a set of instructions that tells the genome how to use the traditional coding genes.
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  • "It's like a recipe book," Wray said. "It tells you how to make the meal. You need to know the amounts. You need to know the order. The noncoding DNA tells you how much to make, when to make it and under what circumstances."
  • common diseases are probably more influenced by regulatory differences, Harismendy said. These include Type 2 diabetes, Crohn's disease, Alzheimer's Disease and a variety of cancers, including breast, colon, ovarian, prostate and lung.
  • According to Wray, research has shown that diseases like bipolar syndrome and clinical depression may be associated with noncoding mutations that determine whether the brain is producing too much or not enough of a particular neurotransmitter. One noncoding mutation gives a person almost complete protection against the nasty malaria parasite, plasmodium vivax.
  • Another piece of noncoding DNA regulates the enzyme responsible for lactose tolerance, the ability to digest milk. Research by Wray and other scientists has shown that in four populations where dairy consumption is a vital part of the diet, new mutations have appeared that essentially keep the gene that produces the lactase enzyme from switching off.
  • And recent research done by evolutionary biologists suggests that differences in regulatory DNA may represent a major part of what separates us from chimpanzees.
orasa sukmark

Junk DNA Can Revive and Cause Disease, Study Finds - NYTimes.com - 0 views

  • can rise from the dead like zombies
  • dead gene come back to life and cause a disease
  • a dead gene come back to life and cause a disease.
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  • Some of those genes, surprised geneticists reported Thursday, can rise from the dead like zombies, waking up to cause one of the most common forms of muscular dystrophy.
    • adisa narula
       
      Do these genes revive automatically?
  • It is a dominant genetic disease.
  • people who have the disease cannot smile.
  • FSHD affects about 1 in 20,000 people
  • function, if any, is largely unknown.
  • function, if any, is largely unknown
  • FSHD, is one of the most common forms of muscular dystrophy.
  • in a way FSHD was the easy case — it is a disease that affects every single person who inherits the genetic defect. Other diseases are more subtle, affecting some people more than others, causing a range of symptoms.
  • The dead gene was also repeated on chromosome 10, but that area of repeats seemed innocuous, unrelated to the disease. Only chromosome 4 was a problem.
  • chromosome 4 was a problem.
  • No one whose dead gene was repeated more than 10 times ever got FSHD
  • it was not completely inactive. It is always transcribed
  • copied by the cell as a first step to making a protein.
  • But the transcriptions were faulty, disintegrating right away. They were missing a crucial section, called a poly (A) sequence, needed to stabilize them.
  • But the transcriptions were faulty, disintegrating right away. They were missing a crucial section, called a poly (A) sequence, needed to stabilize them.
  • extra copies change the chromosome’s structure, shutting off the whole region so it cannot be used.
Nickyz P.

Exercise Brings On DNA Changes - Science News - 2 views

  • These alterations turn on genes that regulate a cell’s energy.
  • Genes can be turned on or off  by a process known as methylation, in which a methyl group — consisting of one carbon atom and three hydrogen atoms — is added to DNA.
nidthamsirisup

Study suggests why some animals live longer - 1 views

    • nidthamsirisup
       
      A new method to detect proteins associated with longevity which helps further our understanding into why some animals live longer than others.
  • The study, led by Dr. Joao Pedro Magalhaes and postgraduate student, Yang Li, is the first to show evolutionary patterns in biological repair systems in long-lived animals and could, in the future, be used to help develop anti-ageing interventions by identifying proteins in long-lived species that better respond to, for example, DNA damage
  • these species have optimised pathways that repair molecular damage, compared to shorter-lived animals, such as mice
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  • found a similar pattern in proteins associated with metabolism, cholesterol and pathways involved in the recycling of proteins
  • Proteins associated with the degradation of damaged proteins, a process that has been connected to ageing, were also linked with the evolution of longevity in mammals.
  • If we can identify the proteins that allow some species to live longer than others we could use this knowledge to improve human health and slow the ageing process.
  • “We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by ageing, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the ageing process.”
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