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Rab proteins comprise a large family of Ras-related GTPases that function in the anterograde and retrograde trafficking of proteins in mammalian cells [ 1 2 3 ] . Different Rab proteins reside in specific subcellular membranes or organelles, where they mediate vesicular transport between discrete donor and acceptor compartments in the endocytic or exocytic pathways [ 4 5 ] . Detailed studies of a few Rab proteins ( e.g .; Rab1, Rab5 and Rab9) have led to a general model wherein Rab proteins are presumed to cycle on and off donor and acceptor membranes in connection with changes in their guanine nucleotide state [ 6 7 8 ] . In the active GTP-bound state, Rab proteins associate with budding transport vesicles [ 9 10 11 ] and appear to participate in the assembly of membrane docking complexes [ 12 13 14 ] . Following vesicle fusion with the acceptor compartment and GTP hydrolysis, the inactive GDP-bound Rab is extracted from the membrane by a carrier protein termed guanine nucleotide dissociation inhibitor (GDI) [ 15 16 17 ] . The GTPase can then re-enter the transport cycle through nucleotide exchange promoted by a specific exchange factor at the donor vesicle membrane [ 18 19 20 ] . In addition to changes in guanine nucleotide state, the posttranslational prenylation of Rab proteins plays an important role in the cycling mechanism.
Progression of granulation tissue to neodermis requires a decrease in cellularity through apoptosis of endothelial cells, fibroblasts and myofibroblasts [ 28 29 ] . Keloid fibroblasts demonstrate aberrant apoptotic behavior [ 30 31 ] although studies have given variable results [ 5 9 11 30 31 32 33 34 35 ] . Our initial data for serum-starvation-induced apoptosis in monolayer cultures of dermal fibroblasts demonstrated delayed apoptosis of keloid fibroblasts and a negative correlation with α-SMA expression [ 36 ] . Similar correlations were observed in rat lung fibroblasts, where TGFβ1 increased α-SMA content while acting as an antiapoptotic agent [ 37 38 ] . It should be noted however, that many of the myofibroblasts were still able to undergo apoptosis consistent with in vivo data on palatal wound healing [ 39 ] . Thus, TGFβ1 can promote both α-SMA expression in the initial stages of wound healing and apoptosis in later stages of wound healing.
These studies, followed by biochemical and structural characterization of these modules has thrown considerable light on the biology of chromatin dynamics and the roles these domains have played in course of evolution [ 14, 15, 16, 20].
The sections were rinsed again and incubated overnight at 4°C with the Rip primary antibody (Developmental Studies Hybridoma Bank, Iowa City, IA; diluted 1:4 in .1 M PBS).
These findings are in accord with previous studies on mouse lung neutrophils during endotoxemia [ 21 ] . Our observation that nuclear binding activity appeared in the cells rapidly after endotoxin administration (within 0.5 hours) indicates that NF-κB and CREB are involved in early functional activation.
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