Source: Johns Hopkins Medicine
Date: April 30, 2012
Summary:
A team of researchers from Johns Hopkins University and the National Human Genome Research Institute has evaluated the whole genomic sequence of stem cells derived from human bone marrow cells -- so-called induced pluripotent stem (iPS) cells -- and found that relatively few genetic changes occur during stem cell conversion by an improved method. The findings, reported in the March issue of Cell Stem Cell, the official journal of the International Society for Stem Cell Research (ISSCR), will be presented at the annual ISSCR meeting in June.
Each time a cell divides, it has the chance to make errors and incorporate new genetic changes in its DNA, Cheng explains. Some genetic changes can be harmless, but others can lead to changes in cell behavior that may lead to disease and, in the worst case, to cancer. In the new study, the researchers showed that iPS cells derived from adult bone marrow cells contain random genetic changes that do not specifically predispose the cells to form cancer.
Showing posts with label cell division. Show all posts
Showing posts with label cell division. Show all posts
Monday, April 30, 2012
Friday, March 23, 2012
Embryonic Stem Cells Shift Metabolism in Cancer-Like Way Upon Implanting in Uterus
Source: University of Washington
Date: March 23, 2012
Summary:
Shortly after a mouse embryo starts to form, some of its stem cells undergo a dramatic metabolic shift to enter the next stage of development, University of Washington researchers have reported. These stem cells start using and producing energy like cancer cells. This discovery is recently published in EMBO, the European Molecular Biology Organization journal.
The metabolic transition they discovered occurs very early as the mouse embryo, barely more than a speck of dividing cells, implants in the mother's uterus. The change is driven by low oxygen conditions, Ruohola-Baker explained.
The researchers also saw a specific type of biochemical slowdown in the stem cells' mitochondria -- the cells' powerhouses. The phenomenon previously was associated with aging and disease. This was the first example of the same downshift controlling normal early embryonic development.
Date: March 23, 2012
Summary:
Shortly after a mouse embryo starts to form, some of its stem cells undergo a dramatic metabolic shift to enter the next stage of development, University of Washington researchers have reported. These stem cells start using and producing energy like cancer cells. This discovery is recently published in EMBO, the European Molecular Biology Organization journal.
The metabolic transition they discovered occurs very early as the mouse embryo, barely more than a speck of dividing cells, implants in the mother's uterus. The change is driven by low oxygen conditions, Ruohola-Baker explained.
The researchers also saw a specific type of biochemical slowdown in the stem cells' mitochondria -- the cells' powerhouses. The phenomenon previously was associated with aging and disease. This was the first example of the same downshift controlling normal early embryonic development.
Wednesday, February 22, 2012
Scientists trigger muscle stem cells to divide
Source: Stanford University School of Medicine
Date: February 22, 2012
Summary:
A tiny piece of RNA plays a key role in determining when muscle stem cells from mice activate and start to divide, according to researchers at the Stanford University School of Medicine. The finding may help scientists learn how to prepare human muscle stem cells for use in therapies for conditions such as muscular dystrophy and aging by controlling their activation state.
It’s the first time that a small regulatory RNA, called a microRNA, has been implicated in the maintenance of the adult stem cell resting, or quiescent, state. The research is published Feb. 23 in Nature. Postdoctoral scholar Tom Cheung, PhD, is the first author of the study.
Date: February 22, 2012
Summary:
A tiny piece of RNA plays a key role in determining when muscle stem cells from mice activate and start to divide, according to researchers at the Stanford University School of Medicine. The finding may help scientists learn how to prepare human muscle stem cells for use in therapies for conditions such as muscular dystrophy and aging by controlling their activation state.
It’s the first time that a small regulatory RNA, called a microRNA, has been implicated in the maintenance of the adult stem cell resting, or quiescent, state. The research is published Feb. 23 in Nature. Postdoctoral scholar Tom Cheung, PhD, is the first author of the study.
Wednesday, November 23, 2011
Key to Aging? Key Molecular Switch for Telomere Extension by Telomerase Identified
Source: University of Illinois at Chicago
Date: November 23, 2011
Summary:
Researchers at the University of Illinois at Chicago College of Medicine describe for the first time a key target of DNA damage checkpoint enzymes that must be chemically modified to enable stable maintenance of chromosome ends by telomerase, an enzyme thought to play a key role in cancer and aging. Their findings are reported online in Nature Structural and Molecular Biology.
Date: November 23, 2011
Summary:
Researchers at the University of Illinois at Chicago College of Medicine describe for the first time a key target of DNA damage checkpoint enzymes that must be chemically modified to enable stable maintenance of chromosome ends by telomerase, an enzyme thought to play a key role in cancer and aging. Their findings are reported online in Nature Structural and Molecular Biology.
Tuesday, September 20, 2011
Scientists Turn Back the Clock On Adult Stem Cells Aging
Source: Georgia Institute of Technology
Date: September 20, 2011
Summary:
Atlanta, GA - Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Date: September 20, 2011
Summary:
Atlanta, GA - Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Monday, September 19, 2011
Scientists Turn Back the Clock on Adult Stem Cells Aging
Source: Buck Institute for Research on Aging
Date: September 19, 2011
Summary:
Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Date: September 19, 2011
Summary:
Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Thursday, May 12, 2011
Pluripotent adult stem cells power planarian regeneration
Source: Whitehead Institute for Biomedical Research
Date: May 12, 2011
Summary:
Researchers at the Whitehead Institute for Biomedical Research have determined that the planarian flatworm regenerates missing tissues by using pluripotent adult stem cells. Until now, scientists could not determine whether the dividing cells in planarians, called neoblasts, are a mixture of specialized stem cells that each regenerates specific tissues, or if individual neoblasts are pluripotent and able to regenerate all tissues. Using complementary methods, the researchers demonstrated that adult planarians not only possess pluripotent stem cells -- known as clonogenic neoblasts (cNeoblasts) -- but that a single such cell is capable of regenerating an entire animal. Their results are published in the May 13 issue of Science.
Date: May 12, 2011
Summary:
Researchers at the Whitehead Institute for Biomedical Research have determined that the planarian flatworm regenerates missing tissues by using pluripotent adult stem cells. Until now, scientists could not determine whether the dividing cells in planarians, called neoblasts, are a mixture of specialized stem cells that each regenerates specific tissues, or if individual neoblasts are pluripotent and able to regenerate all tissues. Using complementary methods, the researchers demonstrated that adult planarians not only possess pluripotent stem cells -- known as clonogenic neoblasts (cNeoblasts) -- but that a single such cell is capable of regenerating an entire animal. Their results are published in the May 13 issue of Science.
Wednesday, May 11, 2011
Human Lung Stem Cell Discovered
Source: Brigham and Women's Hospital
Date: May 11, 2011
Summary:
For the first time, researchers at Brigham and Women's Hospital (BWH) have identified a human lung stem cell that is self-renewing and capable of forming and integrating multiple biological structures of the lung including bronchioles, alveoli and pulmonary vessels. This research is published in the May 12, 2011 issue of the New England Journal of Medicine.
Using lung tissue from surgical samples, researchers identified and isolated the human lung stem cell and tested the functionality of the stem cell both in vitro and in vivo. Once the stem cell was isolated, researchers demonstrated in vitro that the cell was capable of dividing both into new stem cells and also into cells that would grow into various types of lung tissue. Next, researchers injected the stem cell into mice with damaged lungs. The injected stem cells differentiated into new bronchioles, alveoli and pulmonary vessel cells which not only formed new lung tissue, but also integrated structurally to the existing lung tissue in the mice.
Date: May 11, 2011
Summary:
For the first time, researchers at Brigham and Women's Hospital (BWH) have identified a human lung stem cell that is self-renewing and capable of forming and integrating multiple biological structures of the lung including bronchioles, alveoli and pulmonary vessels. This research is published in the May 12, 2011 issue of the New England Journal of Medicine.
Using lung tissue from surgical samples, researchers identified and isolated the human lung stem cell and tested the functionality of the stem cell both in vitro and in vivo. Once the stem cell was isolated, researchers demonstrated in vitro that the cell was capable of dividing both into new stem cells and also into cells that would grow into various types of lung tissue. Next, researchers injected the stem cell into mice with damaged lungs. The injected stem cells differentiated into new bronchioles, alveoli and pulmonary vessel cells which not only formed new lung tissue, but also integrated structurally to the existing lung tissue in the mice.
Tuesday, March 01, 2011
How Long Do Stem Cells Live?
Source: Sanford-Burnham Medical Research Institute
Date: March 1, 2011
Summary:
When patients receive a bone marrow transplant, they are getting a new population of hematopoietic stem cells. Fresh stem cells are needed when a patient is low on red blood cells, as in anemia, or white blood cells, which can be caused by cancer or even cancer treatments such as irradiation or chemotherapy. The problem is that a bone marrow transplant might not succeed because the transplanted stem cells don't live long enough or because they proliferate too well, leading to leukemia.
To help determine how long a bone marrow (stem cell) graft will last, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) have developed a mathematical model that predicts how long a stem cell will live and tested those predictions in a mouse model. The study, led by Christa Muller-Sieburg, Dr. rer. nat., was published online the week of February 28, in the journal Proceedings of the National Academy of Sciences.
Date: March 1, 2011
Summary:
When patients receive a bone marrow transplant, they are getting a new population of hematopoietic stem cells. Fresh stem cells are needed when a patient is low on red blood cells, as in anemia, or white blood cells, which can be caused by cancer or even cancer treatments such as irradiation or chemotherapy. The problem is that a bone marrow transplant might not succeed because the transplanted stem cells don't live long enough or because they proliferate too well, leading to leukemia.
To help determine how long a bone marrow (stem cell) graft will last, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) have developed a mathematical model that predicts how long a stem cell will live and tested those predictions in a mouse model. The study, led by Christa Muller-Sieburg, Dr. rer. nat., was published online the week of February 28, in the journal Proceedings of the National Academy of Sciences.
Thursday, February 03, 2011
Scientists Unlock One Mystery of Tissue Regeneration
Source: University of Rochester
Date: February 3, 2011
Summary:
Researchers at the University of Rochester have now identified a genetic switch that controls oxidative stress in stem cells and thus governs stem cell function. The researchers studied the function of two genes, Nrf2 and Keap1, which were already known as regulators of cellular responses to oxidative stress. The research team was surprised to discover that, in contrast to other cell types, Nrf2 was active within the stem cells even in the absence of stress. This finding suggested that Nrf2 might have an unusual role in the control of stem cell function. The work is being published in the February 4 issue of the scientific journal Cell Stem Cell.
Date: February 3, 2011
Summary:
Researchers at the University of Rochester have now identified a genetic switch that controls oxidative stress in stem cells and thus governs stem cell function. The researchers studied the function of two genes, Nrf2 and Keap1, which were already known as regulators of cellular responses to oxidative stress. The research team was surprised to discover that, in contrast to other cell types, Nrf2 was active within the stem cells even in the absence of stress. This finding suggested that Nrf2 might have an unusual role in the control of stem cell function. The work is being published in the February 4 issue of the scientific journal Cell Stem Cell.
Wednesday, December 15, 2010
Study identifies multitude of genetic regions key to embryonic stem cell development
Source: Stanford University School of Medicine
Date: December 15, 2010
Summary;
More than 2,000 genetic regions involved in early human development have been identified by researchers at the Stanford University School of Medicine. The regions, called enhancers, are responsible for triggering the expression of distant genes when embryonic stem cells begin to divide to form the many tissues of a growing embryo. The research is published online Dec. 15 in Nature.
Date: December 15, 2010
Summary;
More than 2,000 genetic regions involved in early human development have been identified by researchers at the Stanford University School of Medicine. The regions, called enhancers, are responsible for triggering the expression of distant genes when embryonic stem cells begin to divide to form the many tissues of a growing embryo. The research is published online Dec. 15 in Nature.
Wednesday, December 01, 2010
Researchers identify protein essential for cell division in blood-forming stem cells
Source: University of Michigan
Date: December 1, 2010
Summary:
ANN ARBOR, Mich.---University of Michigan researchers have discovered that a protein known to regulate cellular metabolism is also necessary for normal cell division in blood-forming stem cells. Loss of the protein results in an abnormal number of chromosomes and a high rate of cell death. The finding demonstrates that stem cells are metabolically different from other blood-forming cells, which can divide without the protein, Lkb1. This metabolic difference could someday be used to better control the behavior of blood-forming stem cells used in disease treatments, said Sean Morrison, director of the U-M Center for Stem Cell Biology, which is based at the Life Sciences Institute. The researchers deleted the two genes in blood-forming stem cells of mice -- the first time these genes have been "knocked out" in stem cells -- then observed and measured the effects. Their results are reported in the Dec. 2 edition of the journal Nature.
Date: December 1, 2010
Summary:
ANN ARBOR, Mich.---University of Michigan researchers have discovered that a protein known to regulate cellular metabolism is also necessary for normal cell division in blood-forming stem cells. Loss of the protein results in an abnormal number of chromosomes and a high rate of cell death. The finding demonstrates that stem cells are metabolically different from other blood-forming cells, which can divide without the protein, Lkb1. This metabolic difference could someday be used to better control the behavior of blood-forming stem cells used in disease treatments, said Sean Morrison, director of the U-M Center for Stem Cell Biology, which is based at the Life Sciences Institute. The researchers deleted the two genes in blood-forming stem cells of mice -- the first time these genes have been "knocked out" in stem cells -- then observed and measured the effects. Their results are reported in the Dec. 2 edition of the journal Nature.
Wednesday, November 03, 2010
Scientists Find Nerve Cell Activity Drains Stem Cell Pool in Developing Brain
Source: Scripps Research Institute
Date: November 3, 2010
Summary:
As babies grow, their brain cells develop from a pool of stem cells—some stem cells continuously divide, replenishing the pool, whereas others morph into mature functioning nerve cells. Now researchers at The Scripps Research Institute have shown that as the newly formed nerve cells start firing electrical signals, this activity slows down stem cell division, emptying out the stem cell pool in favor of nerve cell formation.
The study, published in the November 4 issue of the journal Neuron, shows that brain activity controls the balance between stem cells and mature nerve cells and suggests that abnormal brain activity, as it occurs during seizures, may have long-lasting effects on brain development. The results also have implications for replacing brain cells that are damaged or lost through diseases such as Alzheimer's or Parkinson's disease.
Date: November 3, 2010
Summary:
As babies grow, their brain cells develop from a pool of stem cells—some stem cells continuously divide, replenishing the pool, whereas others morph into mature functioning nerve cells. Now researchers at The Scripps Research Institute have shown that as the newly formed nerve cells start firing electrical signals, this activity slows down stem cell division, emptying out the stem cell pool in favor of nerve cell formation.
The study, published in the November 4 issue of the journal Neuron, shows that brain activity controls the balance between stem cells and mature nerve cells and suggests that abnormal brain activity, as it occurs during seizures, may have long-lasting effects on brain development. The results also have implications for replacing brain cells that are damaged or lost through diseases such as Alzheimer's or Parkinson's disease.
Wednesday, August 04, 2010
Newts' Ability to Regenerate Tissue Replicated in Mouse Cells
Source: Stanford University
Date: August 4, 2010
Summary:
New research suggests a reason why mammals are unable to re-grow a limb or produce new heart muscle cells: Restricting cells' ability to pop in and out of the cell cycle at will -- a prerequisite for the cell division necessary to make new tissue -- reduces the chances that they'll run amok and form potentially deadly cancers.
Scientists at the Stanford University School of Medicine have taken a big step toward being able to confer this regenerative capacity on mammalian muscle cells; they accomplished this feat in experiments with laboratory mice in which they blocked the expression of just two tumor-suppressing proteins. The finding may move us closer to future regenerative therapies in humans -- surprisingly, by sending us shimmying back down the evolutionary tree. The research will be published in Cell Stem Cell.
Wired magazine published a news story based on this news release.
Date: August 4, 2010
Summary:
New research suggests a reason why mammals are unable to re-grow a limb or produce new heart muscle cells: Restricting cells' ability to pop in and out of the cell cycle at will -- a prerequisite for the cell division necessary to make new tissue -- reduces the chances that they'll run amok and form potentially deadly cancers.
Scientists at the Stanford University School of Medicine have taken a big step toward being able to confer this regenerative capacity on mammalian muscle cells; they accomplished this feat in experiments with laboratory mice in which they blocked the expression of just two tumor-suppressing proteins. The finding may move us closer to future regenerative therapies in humans -- surprisingly, by sending us shimmying back down the evolutionary tree. The research will be published in Cell Stem Cell.
Wired magazine published a news story based on this news release.
Friday, June 25, 2010
Mechanism that may trigger degenerative disease identified
Source: Penn State University
Date: June 25, 2010
Summary:
A mechanism that regulates stem-cell differentiation in mice testes suggests a similar process that may trigger degenerative disease in humans, according to researchers at Penn State University. Research involved manipulating a protein called STAT3 that signals stem cells to decide whether to differentiate into a specialized type of cell or self-renew and remain stem cells. By manipulating STAT3, researchers identified a key regulator of spermatogonial stem cell self-renewal. Every time a stem cell divides, it produces two new cells. The findings were published in the June online issue of Biology of Reproduction.
Date: June 25, 2010
Summary:
A mechanism that regulates stem-cell differentiation in mice testes suggests a similar process that may trigger degenerative disease in humans, according to researchers at Penn State University. Research involved manipulating a protein called STAT3 that signals stem cells to decide whether to differentiate into a specialized type of cell or self-renew and remain stem cells. By manipulating STAT3, researchers identified a key regulator of spermatogonial stem cell self-renewal. Every time a stem cell divides, it produces two new cells. The findings were published in the June online issue of Biology of Reproduction.
Monday, March 15, 2010
SCIENTISTS DEMONSTRATE MAMMALIAN REGENERATION THROUGH A SINGLE GENE DELETION
Source: The Wistar Institute
Date: March 15, 2010
Summary:
A quest that began over a decade ago with a chance observation has reached a milestone: the identification of a gene that may regulate regeneration in mammals. The absence of this single gene, called p21, confers a healing potential in mice long thought to have been lost through evolution and reserved for creatures like flatworms, sponges, and some species of salamander. In a report published today in the Proceedings of the National Academy of Sciences, researchers from The Wistar Institute demonstrate that mice that lack the p21 gene gain the ability to regenerate lost or damaged tissue.
Unlike typical mammals, which heal wounds by forming a scar, these mice begin by forming a blastema, a structure associated with rapid cell growth and de-differentiation as seen in amphibians. According to the Wistar researchers, the loss of p21 causes the cells of these mice to behave more like embryonic stem cells than adult mammalian cells, and their findings provide solid evidence to link tissue regeneration to the control of cell division.
Date: March 15, 2010
Summary:
A quest that began over a decade ago with a chance observation has reached a milestone: the identification of a gene that may regulate regeneration in mammals. The absence of this single gene, called p21, confers a healing potential in mice long thought to have been lost through evolution and reserved for creatures like flatworms, sponges, and some species of salamander. In a report published today in the Proceedings of the National Academy of Sciences, researchers from The Wistar Institute demonstrate that mice that lack the p21 gene gain the ability to regenerate lost or damaged tissue.
Unlike typical mammals, which heal wounds by forming a scar, these mice begin by forming a blastema, a structure associated with rapid cell growth and de-differentiation as seen in amphibians. According to the Wistar researchers, the loss of p21 causes the cells of these mice to behave more like embryonic stem cells than adult mammalian cells, and their findings provide solid evidence to link tissue regeneration to the control of cell division.
Sunday, August 09, 2009
New steps forward in cell reprogramming
Source: Harvard University
Date: August 9, 2009
Summary:
Harvard Stem Cell Institute (HSCI) researchers at Massachusetts General Hospital (MGH) have substantially improved the odds of successfully reprogramming differentiated cells into induced pluripotent stem cells (iPS) by blocking the activity of the gene that instructs the cells to stop dividing.
Konrad Hochedlinger and colleagues at the MGH Center for Regenerative Medicine also found that reprogramming efforts are more likely to be successful if they target immature cells rather than their more mature counterparts for reprogramming.
Induced pluripotent cells are adult cells that have been reprogrammed back to an embryo-like state in which they have regained the potential to turn into any of the 220 cell types in the body, such as liver cells, skin cells, or heart cells. “This has been a main question and main interest in the field for a long time,” says Hochedlinger. “When you work with mature cells, for some reason only a few of them actually reprogram into an iPS cell: Why is the reprogramming process so inefficient?”
The team has devised two solutions for the problem of inefficiency, one of which involves selecting only certain cell types for reprogramming. The work is being published in two separate reports, one in the journal Nature, and the other in Nature Genetics.
Date: August 9, 2009
Summary:
Harvard Stem Cell Institute (HSCI) researchers at Massachusetts General Hospital (MGH) have substantially improved the odds of successfully reprogramming differentiated cells into induced pluripotent stem cells (iPS) by blocking the activity of the gene that instructs the cells to stop dividing.
Konrad Hochedlinger and colleagues at the MGH Center for Regenerative Medicine also found that reprogramming efforts are more likely to be successful if they target immature cells rather than their more mature counterparts for reprogramming.
Induced pluripotent cells are adult cells that have been reprogrammed back to an embryo-like state in which they have regained the potential to turn into any of the 220 cell types in the body, such as liver cells, skin cells, or heart cells. “This has been a main question and main interest in the field for a long time,” says Hochedlinger. “When you work with mature cells, for some reason only a few of them actually reprogram into an iPS cell: Why is the reprogramming process so inefficient?”
The team has devised two solutions for the problem of inefficiency, one of which involves selecting only certain cell types for reprogramming. The work is being published in two separate reports, one in the journal Nature, and the other in Nature Genetics.
Thursday, August 06, 2009
What Makes Stem Cells Tick? Researchers Identify Phosphorylated Signaling Proteins in Human Embryonic Stem Cells
Source: Burnham Institute for Medical Research
Date: August 6, 2009
Summary:
LA JOLLA, Calif., -- Investigators at the Burnham Institute for Medical Research (Burnham) and The Scripps Research Institute (TSRI) have made the first comparative, large-scale phosphoproteomic analysis of human embryonic stem cells (hESCs) and their differentiated derivatives. The data may help stem cell researchers understand the mechanisms that determine whether stem cells divide or differentiate, what types of cells they become and how to control those complex mechanisms to facilitate development of new therapies. The study was published in the August 6 issue of the journal Cell Stem Cell.
Date: August 6, 2009
Summary:
LA JOLLA, Calif., -- Investigators at the Burnham Institute for Medical Research (Burnham) and The Scripps Research Institute (TSRI) have made the first comparative, large-scale phosphoproteomic analysis of human embryonic stem cells (hESCs) and their differentiated derivatives. The data may help stem cell researchers understand the mechanisms that determine whether stem cells divide or differentiate, what types of cells they become and how to control those complex mechanisms to facilitate development of new therapies. The study was published in the August 6 issue of the journal Cell Stem Cell.
Scientists find common trigger in cancer and normal stem cell reproduction
Source: Stanford University Medical Center
Date: August 6, 2009
Summary:
STANFORD, Calif. — Researchers at Stanford University School of Medicine have discovered, for the first time, a common molecular pathway that is used by both normal stem cells and cancer stem cells when they reproduce themselves. In a paper to be published Aug. 7 in the journal Cell, Michael Clarke, MD, the Karel H. and Avice N. Beekhuis Professor in Cancer Biology, and his colleagues showed that breast cancer stem cells and normal breast stem cells turn down the creation of a specific group of cell signals when they are reproducing. Increasing the amount of one of these signals, called miR-200c, strongly suppressed the ability of both cancer stem cells and normal stem cells to divide and reproduce. The discovery of a common regulatory pathway in both kinds of stem cells supports the idea that cancer stem cells and normal stem cells share fundamental properties.
Date: August 6, 2009
Summary:
STANFORD, Calif. — Researchers at Stanford University School of Medicine have discovered, for the first time, a common molecular pathway that is used by both normal stem cells and cancer stem cells when they reproduce themselves. In a paper to be published Aug. 7 in the journal Cell, Michael Clarke, MD, the Karel H. and Avice N. Beekhuis Professor in Cancer Biology, and his colleagues showed that breast cancer stem cells and normal breast stem cells turn down the creation of a specific group of cell signals when they are reproducing. Increasing the amount of one of these signals, called miR-200c, strongly suppressed the ability of both cancer stem cells and normal stem cells to divide and reproduce. The discovery of a common regulatory pathway in both kinds of stem cells supports the idea that cancer stem cells and normal stem cells share fundamental properties.
Thursday, May 14, 2009
How an enzyme tells stem cells which way to divide
Source: University of Oregon
Date: May 14, 2009
Summary:
Driving Miranda, a protein in fruit flies crucial to switch a stem cell's fate, is not as complex as biologists thought, according to University of Oregon biochemists. They've found that one enzyme (aPKC) stands alone and acts as a traffic cop that directs which roads daughter cells will take.
"Wherever aPKC is at on a cell's cortex or membrane, Miranda isn't," says Kenneth E. Prehoda, a professor in the chemistry department and member of the University of Oregon's Institute of Molecular Biology. When a stem cell duplicates into daughter cells, the side, or cortical domain, containing aPKC (atypical protein kinase C) continues as a stem cell, while the other domain with Miranda becomes a differentiated cell such as a neuron that forms the central nervous system.
Prehoda and co-author Scott X. Atwood, who studied in Prehoda's lab and recently earned his doctorate, describe how the mechanism works in the May 12 issue of the journal Current Biology.
Date: May 14, 2009
Summary:
Driving Miranda, a protein in fruit flies crucial to switch a stem cell's fate, is not as complex as biologists thought, according to University of Oregon biochemists. They've found that one enzyme (aPKC) stands alone and acts as a traffic cop that directs which roads daughter cells will take.
"Wherever aPKC is at on a cell's cortex or membrane, Miranda isn't," says Kenneth E. Prehoda, a professor in the chemistry department and member of the University of Oregon's Institute of Molecular Biology. When a stem cell duplicates into daughter cells, the side, or cortical domain, containing aPKC (atypical protein kinase C) continues as a stem cell, while the other domain with Miranda becomes a differentiated cell such as a neuron that forms the central nervous system.
Prehoda and co-author Scott X. Atwood, who studied in Prehoda's lab and recently earned his doctorate, describe how the mechanism works in the May 12 issue of the journal Current Biology.
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