Sentence examples for autonomous survival from inspiring English sources

The low thymic cellularity is due to massive apoptosis of thymocytes resulting from an autonomous survival defect [14], which has not been seen in single knockout models [7], [6], suggesting a redundant function between these two Egr molecules.

Together with our acute TACI-Ig depletion experiments, this confirms that combined Bim and Bmf deficiency does provide a cell autonomous survival advantage to B cells in the absence of BAFF.

These results indicate that suppression of apoptosis promotes autonomous survival of lymphoma cells but compromises additional pro-tumor mechanisms, which are otherwise generated by apoptotic B lymphoma cells in vivo.

Furthermore, filamin-A is dispensable for cell-autonomous survival and loss of filamin-A expression or depletion of filamin-A with RNAi does not cause cell death or not impede growth [ 88, 125- 127].

In summary, we have shown that VEGF164 is a cell-autonomous survival factor for developing GnRH neurons that signals through NRP1 and cooperates with SEMA3A-mediated axon guidance to ensure the normal development of the neuroendocrine system that regulates sexual reproduction.

Thus, controlling the neuronal defect and subsequent cell-autonomous survival or death of discrete neurons in a diseased animal offers a powerful tool to investigate the developmental and behavioral effects of restoring or maintaining normal aspects of neuronal network function in a disease setting (Fig. 3).

In addition, paracrine signaling of FGF10 promoted androgen independent survival of a subset of prostate adenocarcinoma, and also synergizes with epithelial autonomous AKT signaling, leading to high-grade carcinoma [ 143].

These lipid autacoids may be involved in cancer in a few different ways: either in cell-autonomous tumor survival and growth or in modulating stromal processes, such as angiogenesis and inflammation that can support tumor progression.

Genetic alterations in many of the known oncogenes are selected to adapt cellular metabolism to meet the requirements of rapid cell proliferation as well as autonomous growth and survival in an environment absent of contact with extracellular matrix.

A plethora of mechanistic studies in particular in colorectal cancer models describe how COX-2 may impact on cancer cell-autonomous proliferative and survival signals as well as the microenvironment.

Accordingly, we propose that the accelerated lymphoma development in bim−/− bad−/− animals may reflect a concomitant cell-autonomous enhancement of survival in immature thymocytes, mediated largely by the absence of Bim, and a hematopoietic-extrinsic contribution by a more robust stromal support population, promoted primarily by the absence of Bad.