Katherine H Schreiber studies how certain chemicals from the immune system can harm insulin-producing cells in the pancreas, which are crucial for controlling blood sugar levels. Specifically, she looks at how these chemicals trigger a response that leads to the production of nitric oxide, a molecule that damages the DNA of these cells. This research is important because it enhances our understanding of type 1 diabetes, a condition where the immune system mistakenly attacks and destroys these vital cells. By identifying the processes involved, her work aims to find new protective strategies or treatments to help prevent this disease.
Key findings
Cytokines from the immune system induce the production of nitric oxide, which damages DNA in pancreatic β cells.
The presence of ATM protein (Ataxia Telangiectasia Mutated) promotes self-destruction (apoptosis) of the damaged pancreatic cells instead of repairing them.
This research provides insight that could lead to better protective methods for insulin-producing cells, potentially improving outcomes for type 1 diabetes patients.
Frequently asked questions
Does Dr. Schreiber study type 1 diabetes?
Yes, her research specifically focuses on how the immune system destroys insulin-producing cells in type 1 diabetes.
What mechanisms does Dr. Schreiber explore in her research?
She explores how immune chemicals like cytokines interact with pancreatic cells and induce damaging responses.
Can Dr. Schreiber's findings lead to new treatments?
Yes, by understanding the processes involved in cell destruction, her work may help develop new treatments to protect pancreatic cells from damage.
Publications in plain English
Modulating FKBP5/FKBP51 and autophagy lowers HTT (huntingtin) levels.
Plain English This study looked at a protein called FKBP5 and its role in Huntington's disease, which is a neurological disorder. Researchers found that levels of FKBP5 were lower in mouse models of the disease and that reducing FKBP5 helped to lower the levels of the harmful mutant huntingtin protein by boosting the cell's natural cleanup processes. Specifically, they reported that after using a drug called SAFit2 for two weeks, they achieved a significant decrease in mutant huntingtin levels in mouse models.
Who this helps: This research benefits patients with Huntington's disease by identifying potential new treatment targets.
A novel rapamycin analog is highly selective for mTORC1 in vivo.
2019
Nature communications
Schreiber KH, Arriola Apelo SI, Yu D, Brinkman JA, Velarde MC +11 more
Plain English Researchers studied a new drug called DL001, which is a more targeted version of rapamycin that specifically inhibits a protein complex known as mTORC1 while avoiding unwanted effects on other cellular processes. They found that DL001 is 40 times more selective for mTORC1 than rapamycin and can reduce harmful side effects related to metabolism and the immune system, making it a promising option for treating age-related diseases without the negative impacts seen with traditional rapamycin. This is important because it could lead to safer treatments that help people live healthier for longer.
Who this helps: Patients, especially those with age-related diseases.
Nucleo-cytoplasmic Partitioning of ARF Proteins Controls Auxin Responses in Arabidopsis thaliana.
2019
Molecular cell
Powers SK, Holehouse AS, Korasick DA, Schreiber KH, Clark NM +9 more
Plain English This study looked at how specific proteins called ARFs help plants respond to a growth hormone called auxin. The researchers found that two proteins, ARF7 and ARF19, cluster together in the cell's cytoplasm when the plant isn't responding strongly to auxin. They discovered that a small change in one part of these proteins can cause them to move into the cell's nucleus, which changes how the plant genes behave and affects the plant's growth.
Who this helps: This helps plant scientists and agricultural researchers.
Plain English The researchers studied how a specific signaling pathway, called mTORC1, affects the health and maintenance of stem cells in the body during times when the body needs to regenerate tissues, like after injury. They found that while this signaling helps stem cells multiply quickly when needed, repeated activation during recovery can actually lead to the loss of these cells. For example, they discovered that preventing mTORC1 activation in mice could stop age-related loss of stem cells, meaning these cells can be preserved better as organisms get older.
Who this helps: This research benefits patients, especially the elderly, by providing insights into how to maintain healthy stem cells during aging and injury.
Rapamycin-mediated mTORC2 inhibition is determined by the relative expression of FK506-binding proteins.
2015
Aging cell
Schreiber KH, Ortiz D, Academia EC, Anies AC, Liao CY +1 more
Plain English This study focused on how the drug rapamycin affects specific parts of a pathway related to cancer and aging. Researchers found that the levels of two proteins, FKBP12 and FKBP51, play a crucial role in whether rapamycin can inhibit a pathway called mTORC2, which is linked to negative side effects. For example, reducing FKBP12 made cells that usually respond to rapamycin less sensitive to its effects, while lowering FKBP51 had the opposite effect.
Who this helps: This research benefits patients with cancer and age-related diseases by potentially improving treatment strategies.
Nitric oxide induces ataxia telangiectasia mutated (ATM) protein-dependent γH2AX protein formation in pancreatic β cells.
2014
The Journal of biological chemistry
Oleson BJ, Broniowska KA, Schreiber KH, Tarakanova VL, Corbett JA
Plain English Researchers found that when immune chemicals called cytokines attack insulin-producing cells in the pancreas, they trigger a molecular signal (nitric oxide) that damages the cells' DNA and activates a protein called ATM. Rather than repairing this damage, the ATM protein actually helps push the injured cells toward self-destruction (apoptosis).
This matters because it explains how the immune system destroys the insulin-producing cells in type 1 diabetes, which could eventually lead to better ways to protect those cells or prevent the disease.
When lamins go bad: nuclear structure and disease.
2013
Cell
Schreiber KH, Kennedy BK
Plain English This research paper examines how problems with nuclear lamins, which are proteins that help support the cell's nucleus, lead to a variety of genetic diseases known as laminopathies. These diseases can cause conditions like muscular dystrophy, nerve damage, and signs of premature aging. The study highlights advances in understanding how these nuclear structure issues affect cell function and suggests that new small molecules could be developed as potential treatments.
Who this helps: This benefits patients suffering from laminopathies and their related conditions.
Chronic rapamycin treatment or lack of S6K1 does not reduce ribosome activity in vivo.
2013
Cell cycle (Georgetown, Tex.)
Garelick MG, Mackay VL, Yanagida A, Academia EC, Schreiber KH +2 more
Plain English This study looked at how chronic treatment with the drug rapamycin and the absence of a protein called S6K1 affect protein making in mice. They found that while a single dose of rapamycin reduced protein production, multiple doses over four weeks did not change it at all, and mice without S6K1 showed no difference in protein production compared to normal mice. This is important because it suggests that the health benefits of rapamycin and S6K1 might not come from lowering overall protein production, but rather from targeted changes in specific processes within the cell.
Who this helps: This helps researchers studying aging and longevity in medicine.
The ribosomal protein Rpl22 controls ribosome composition by directly repressing expression of its own paralog, Rpl22l1.
2013
PLoS genetics
O'Leary MN, Schreiber KH, Zhang Y, Duc AC, Rao S +12 more
Plain English This study focused on a protein called Rpl22 in mice and how it influences another similar protein, Rpl22l1. The researchers found that when Rpl22 was removed from mice, the body responded by increasing Rpl22l1 levels, showing that both proteins can support cell growth. This is important because it reveals that ribosomes in mammals might have unique compositions similar to those in yeast, indicating that understanding these proteins can help us learn more about ribosome function.
Who this helps: This helps scientists and researchers studying protein functions in cells.
Rapamycin reverses elevated mTORC1 signaling in lamin A/C-deficient mice, rescues cardiac and skeletal muscle function, and extends survival.
2012
Science translational medicine
Ramos FJ, Chen SC, Garelick MG, Dai DF, Liao CY +8 more
Plain English Researchers studied mice lacking a specific gene, LMNA, which is linked to various diseases that affect muscles and the heart. They found that giving these mice a drug called rapamycin reduced harmful signaling in their cells, improved their heart and muscle function, and increased their lifespan; in fact, the drug helped reduce abnormal protein buildup in heart and muscle tissues. This is important because it highlights a potential treatment strategy for diseases caused by LMNA mutations.
Who this helps: This benefits patients with laminopathies, including those with muscle and heart disorders.