Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.3.1.108 (
TAT
)
2,389
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The phenotypes of mice lacking peptidyl prolyl cis/trans isomerase
Pin1
(
Pin1
(-/-)) indicated that deficient
Pin1
might be related to a variety of diseases. We created
TAT
-
Pin1
, a fusion protein of human immunodeficiency virus 1 trans-activator of transcription factor with
Pin1
. Treatment of HeLa cells with
TAT
-
Pin1
increased the ratio of the S phase. Moreover,
TAT
-
Pin1
restored the proliferating function of
Pin1
(-/-) mouse embryonic fibroblasts which cannot restart proliferation after G0 arrest. These results indicate that
TAT
-
Pin1
is useful in studying the functions of
Pin1
and can be developed as a macromolecular drug for diseases related to
Pin1
loss.
...
PMID:Preparation of protein transduction domain-fused peptidyl prolyl cis/trans isomerase Pin1. 2094 14
This study tested the hypothesis that priming the neutrophil respiratory burst requires both granule exocytosis and activation of the prolyl isomerase
Pin1
. Fusion proteins containing the
TAT
cell permeability sequence and either the SNARE domain of syntaxin-4 or the N-terminal SNARE domain of SNAP-23 were used to examine the role of granule subsets in TNF-mediated respiratory burst priming using human neutrophils. Concentration-inhibition curves for exocytosis of individual granule subsets and for priming of fMLF-stimulated superoxide release and phagocytosis-stimulated H2O2 production were generated. Maximal inhibition of priming ranged from 72 to 88%. Linear regression lines for inhibition of priming versus inhibition of exocytosis did not differ from the line of identity for secretory vesicles and gelatinase granules, while the slopes or the y-intercepts were different from the line of identity for specific and azurophilic granules. Inhibition of
Pin1
reduced priming by 56%, while exocytosis of secretory vesicles and specific granules was not affected. These findings indicate that exocytosis of secretory vesicles and gelatinase granules and activation of
Pin1
are independent events required for TNF-mediated priming of neutrophil respiratory burst.
...
PMID:Exocytosis of neutrophil granule subsets and activation of prolyl isomerase 1 are required for respiratory burst priming. 2336 74