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1 iously cloned and shown to interact with the HIV Tat protein.
2 creased by treatment of cells with exogenous HIV-tat protein.
3 rming the chemotactic characteristics of the HIV-Tat protein.
6 ences basal HIV gene expression and that the HIV Tat protein activates transcription independently of
8 in transduction domain (PTD) embedded in the HIV TAT protein (amino acids 47-57) has been shown to su
9 Formation of a specific complex between the HIV Tat protein and the small RNA element TAR is critica
10 f (ARM) of the human immunodeficiency virus (HIV) Tat protein and TAR RNA is essential for Tat activa
12 the protein transduction domain (PTD) of the HIV/TAT protein and transduced pancreatic islets ex vivo
13 n of NF-kappa B, AP-1, JNK, and apoptosis by HIV-tat protein but has minimal or no role in activation
16 man histiocytic lymphoma U937 cells with the HIV-tat protein causes activation of JNK and AP-1 in a t
17 se ApiCCT1 has a region of similarity to the HIV Tat protein cell-transduction domain, we tested whet
19 glutathione peroxidase, NK-lysin/granulysin, HIV Tat protein, H(2)O(2), lipid hydroperoxides, vitamin
20 nstrated that a TAT peptide derived from the HIV TAT protein has the ability to transduce peptides or
24 ot only further highlights the importance of HIV Tat protein in HIV/neuroAIDS, but also presents a ne
28 Treatment of primary monocytes with soluble HIV-Tat protein is associated with increased monocyte me
31 Treatment of primary monocytes with soluble HIV-Tat protein mimicked many of the properties of HIV i
32 , we demonstrated that exposure of HUVECs to HIV Tat protein resulted in induced expression of cell a
33 n or treatment with a CRMP2 peptide fused to HIV TAT protein (TAT-CBD3) blocked neuronal death follow
34 ugated to the protein transduction domain of HIV-TAT protein (TATFLAGVHL-peptide) to facilitate entry
35 l-penetrating peptide (CPP) conjugate of the HIV TAT protein that is fused to an aminoterminal sequen
37 The conjugation of peptides derived from the HIV TAT protein to membrane-impermeant molecules has gai
39 but continues to synergize normally with the HIV Tat protein to transactivate the HIV long terminal r
40 argeted by the human immunodeficiency virus (HIV) Tat protein to activate elongation of the integrate
41 t study, we have examined the ability of the HIV-Tat protein to alter the migratory and invasive beha
42 tumor-associated Ag (OVA) that contains the HIV TAT protein transduction domain (PTD) was readily en
43 s with versions of these peptides containing HIV-Tat protein transduction and mammalian mitochondrial
44 f class IA PI3K adaptor subunit, fused to an HIV-TAT protein transduction domain (TAT-Deltap85) conce
47 ibitors of transcriptional activation by the HIV Tat protein, we used a combination of in vitro and i
48 Lipopolysaccharide (LPS) and the neurotoxic HIV Tat protein, which cause dopamine neuronal toxicity
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