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STAT3-mediated transcription of Bcl-2, Mcl-1 and c-IAP2 prevents apoptosis in polyamine-depleted cells.
TLDR
It is suggested that activation of STAT3 in response to polyamine depletion increases the transcription and subsequent expression of anti-apoptotic Bcl-2 and IAP family proteins and thereby promotes survival of cells against TNF-alpha-induced apoptosis.
Lysophosphatidic Acid Induces Neointima Formation Through PPARγ Activation
TLDR
Exposure to brief exposure to either alkyl ether analogs of the growth factor–like phospholipid lysophosphatidic acid (LPA), products generated during the oxidative modification of low density lipoprotein, or to unsaturated acyl forms of LPA induce progressive formation of neointima in vivo in a rat carotid artery model suggests selected LPA analogs are important novel endogenous PPARγ ligands capable of mediating vascular remodeling.
Decreased expression of protooncogenes c-fos, c-myc, and c-jun following polyamine depletion in IEC-6 cells.
TLDR
Treatment with DFMO not only prevented increased expression of c-myc and c-jun protooncogenes at 4 days, but also significantly reduced steady-state levels of c, myc andc-jun mRNA between 6 and 12 days.
Migration of IEC-6 cells: a model for mucosal healing.
Cell migration is the principal force behind the early restitution of erosions of the mucosa of the gastrointestinal tract. Despite the importance of cell migration to healing, no attempts to study
Regulation of gastrointestinal mucosal growth
  • L. Johnson
  • Medicine
    World Journal of Surgery
  • 1 July 1979
TLDR
The possible mechanisms initiated by the ingestion and presence of food in the digestive tract that might regulate the growth of gastrointestinal mucosa are reviewed, with emphasis on direct local nutrition, pancreatic and biliary secretions, and gastrointestinal hormones.
Rho proteins play a critical role in cell migration during the early phase of mucosal restitution.
TLDR
It is demonstrated that Rho is required for endogenous and EGF-induced migration of small intestinal crypt cells, and that RHo proteins are essential elements of a mechanism by which growth factors induce cell migration to restitute mucosal integrity.
Polyamine depletion arrests cell cycle and induces inhibitors p21(Waf1/Cip1), p27(Kip1), and p53 in IEC-6 cells.
TLDR
The results indicate that polyamine depletion causes cell cycle arrest and upregulates cell cycle inhibitors and suggest that MAPK and JNK may be involved in the regulation of the activity of these molecules.
Stimulation of proximal small intestinal mucosal growth by luminal polyamines.
TLDR
Administration of the polyamines significantly reversed the effects of DFMO except the inhibition of ODC and there were no significant differences in mucosal growth parameters between the controls (without DFMO) and those treated with DFMO plus polyamines.
Essential Medical Physiology
General physiology cardiovascular physiology respiratory physiology renal physiology gastrointestinal physiology endocrine physiology central nervous system physiology.
Protein Phosphatase 2A Regulates Apoptosis in Intestinal Epithelial Cells*
TLDR
It is shown that polyamine depletion inhibits serine/threonine phosphatase 2A (PP2A) activity, and inhibition of PP2A in response to polyamines depletion increases steady state levels of Bad and Bcl-2 proteins and their phosphorylation and thereby prevents cytochrome c release, caspases-9, and caspase-3 activation.
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