LDR 02094nab a2200229z? 4500
003 1997-10-07 15:11:57.0
005 2009-10-13 22:24:37.0
008 950724|1996||||pr || ||||||| 0|||||eng|d
082 00$aSalud y medicina
245 00$aMolecular mechanisms of angiogenesis:$bExperimental models define cellular trafficking of FGF-1
260 $aPUERTO RICO HEALTH SCIENCES JOURNAL,$c15 (3) Sept. 1996: 179-186. bibl. fotos.
440 0$aPuerto Rico health sciences journal,$nvol. 15, núm. 3; Sept. 1996
500 $aKey words: Fibroblast growth factor, Fibroblast growth factor, receptor Retroviral gene transfer, Transgenic techniques, Cell transformation, Nuclear transport, Lens differentiation, HIV-1 TAT, Oxidative stress.
520 $aNumerous studies have established that stimulation of cell growth by members of the fibroblast growth (FGF) family of polypeptides is dependent upon an extracellular pathway. Acidic FGF (FGF-1), however, lacks a classical signal sequence for secretion, thereby making it difficult to evaluate regulation of biological activity by this growth factor.
520 $aEfforts in this laboratory have utilized molecular techniques of retrovirology and transgenic modeling to introduce cDNA sequences encoding either an intracellular or extracellular form of FGF-1 into primary diploid cells to examine trafficking and compartmentalization of FGF-1.
520 $aSeveral lines of evidence obtained from these models provide a compelling argument that the stimulation of FGF-1-associated cellular transformation is restricted to an extracellular, receptor-mediated pathway, involving protein tyrosine phosphorylation and nuclear localization. In addition, an unconventional secretion pathway for intracellular FGF-1 has been identified that involves mechanisms associated with oxidative stess.
700 1 $aHicks, Kristine K.
700 1 $aShin, Jordan T.
700 1 $aOpalenik, Susan R.
700 1 $aThompson, John A.
999 0 $luci$kgnrv$s1$wh$aSalud y$bmedicina$mc. 1$61$ePida la revista citada en el renglon "REVISTA".$zNCC:D$xci$hpp$gcirv$nddc