Publications by authors named "A M Dieterle"
Article Synopsis
- Antibody-mediated rejection (AMR) is a big problem for people who have had kidney transplants because it can happen anytime and is caused by antibodies from the donor.
- Sometimes it's hard to find out exactly which donor the antibodies are from because doctors can't always get the donor's DNA or the right tests.
- Researchers found a solution by using urine from the transplant patients to grow donor kidney cells, which helped them get good DNA and figure out the right donor match, proving it's a useful way to check for problems like AMR.
Article Synopsis
- The organ shortage demands careful evaluation of postmortem organs and efforts to extend transplanted organ lifespans.
- Many centers are now accepting organs that meet extended criteria due to the lack of available organs.
- A case study of a kidney transplant is presented, identifying a rare genetic condition in the donor that contributed to chronic transplant function decline, but ultimately resulted in successful long-term outcomes for five recipients.
The PI3K/PDK1/Akt signaling axis is centrally involved in cellular homeostasis and controls cell growth and proliferation. Due to its key function as regulator of cell survival and metabolism, the dysregulation of this pathway is manifested in several human pathologies including cancers and immunological diseases. Thus, current therapeutic strategies target the components of this signaling cascade.
View Article and Find Full Text PDFUnder normal growth conditions the mammalian target of rapamycin complex 1 (mTORC1) negatively regulates the central autophagy regulator complex consisting of Unc-51-like kinases 1/2 (Ulk1/2), focal adhesion kinase family-interacting protein of 200 kDa (FIP200) and Atg13. Upon starvation, mTORC1-mediated repression of this complex is released, which then leads to Ulk1/2 activation. In this scenario, Atg13 has been proposed as an adaptor mediating the interaction between Ulk1/2 and FIP200 and enhancing Ulk1/2 kinase activity.
View Article and Find Full Text PDFThe protein kinase inhibitor staurosporine is one of the most potent and frequently used proapoptotic stimuli, although its mechanism of action is poorly understood. Here, we show that staurosporine as well as its analog 7-hydroxystaurosporine (UCN-01) not only trigger the classical mitochondrial apoptosis pathway but, moreover, activate an additional novel intrinsic apoptosis pathway. Unlike conventional anticancer drugs, staurosporine and UCN-01 induced apoptosis in a variety of tumor cells overexpressing the apoptosis inhibitors Bcl-2 and Bcl-x(L).
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