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1 AT comprises two essential subunits, SET and pp32.
2 t also contains the tumor suppressor protein pp32.
3 djacent benign prostate continues to express pp32.
4 e cloning of cDNAs encoding human and murine pp32.
5      In contrast, constitutive expression of pp32 abolishes ras mediated transformation in vitro and
6 emonstrate, from the functional aspect, that pp32 acts as a tumor suppressor.
7               Two cellular proteins, SET and pp32, also associated with viral DNA during early phase.
8 fers in this region through truncation after pp32 amino acid 131.
9 truncation analysis define a region spanning pp32 amino acids 150-174 as absolutely required for inhi
10                                 We show that pp32 and APRIL are nucleocytoplasmic shuttling proteins
11 tain long, acidic COOH-terminal tails, while pp32 and APRIL share a second motif: rev-like leucine-ri
12 ptomycin B leads to the nuclear retention of pp32 and APRIL, their increased association with HuR, an
13 he other involves two protein ligands of HuR-pp32 and APRIL-which contain leucine-rich nuclear export
14                                 Reduction of pp32 and consequent differentiation were accompanied by
15                           We used anti-sense pp32 and RNAi transfection to study the effects of reduc
16 teraction inhibits the apoptotic activity of pp32 and stimulates proliferation.
17 x also contains the tumor suppressor protein pp32 and the granzyme A-activated DNase NM23-H1, which i
18 D) is in an ER associated complex containing pp32 and the GzmA substrates SET, HMG-2, and Ape1.
19 sm and to stabilize mRNA: SETalpha, SETbeta, pp32, and acidic protein rich in leucine (APRIL).
20 e assembly protein SET, the tumor suppressor pp32, and the base excision repair enzyme APE can induce
21 andscape of the leucine-rich repeat protein, pp32 (Anp32), obtained by combining pressure-dependent s
22                                              pp32 (ANP32A) is a nuclear phosphoprotein expressed as a
23                                              pp32 (ANP32A) is a pro-apoptotic nuclear phosphoprotein,
24        NIH3T3 cells with antisense-inhibited pp32 are not tumorigenic, but are markedly more suscepti
25                   Finally, Set/TAF-Ibeta and pp32 associate with an endogenous estrogen receptor-regu
26              Additionally, Set/TAF-Ibeta and pp32 associate with histone deacetylases in vitro and in
27     In this study, we identify the region of pp32 associated with the ability to inhibit oncogene-med
28             We demonstrate that both SET and pp32 bind directly to the N terminus of H3.
29 t that hyperphosphorylated Rb interacts with pp32 but not with the closely related proteins pp32r1 an
30 ss high levels of the nuclear phosphoprotein pp32 by in situ hybridization.
31 n in expression of SET, which complexes with pp32, by a marked change in acetylation status of histon
32 at the histone binding and INHAT activity of pp32 can be regulated by its physical association with o
33                             Human and murine pp32 cDNAs are 88% identical; the predicted proteins are
34  antibodies with higher affinity for phospho-pp32 demonstrate that pp32 is indeed phosphorylated in v
35 p32 is suggestive of a transcription factor, pp32 did not significantly modulate transcription of a r
36    This family includes the tumor suppressor pp32, expressed in normal tissue, and the pro-oncogenic
37 transfection to study the effects of reduced pp32 expression in the TSU-Pr1 carcinoma cell line.
38 ervations, we hypothesized that reduction of pp32 expression might be an important differentiation si
39 ernative use of genes of the closely-related pp32 family is a common occurrence in human prostate can
40 te the pathways and mechanisms through which pp32 family members exert their functions.
41 2r1 and pp32r2, the oncogenic members of the pp32 family, are expressed in prostatic adenocarcinoma,
42 d in part by alternative use of genes of the pp32 family.
43                 Furthermore, inactivation of pp32 function through alternative gene use may be a crit
44            Prostatic adenocarcinomas express pp32 in a differentiation related manner-well-differenti
45  We demonstrate that antisense inhibition of pp32 in NIH3T3 cells leads to a variety of phenotypic ch
46                           Thus, reduction of pp32 in the undifferentiated TSU-Pr1 neoplastic cell lin
47          This study focuses upon the role of pp32 in tumor suppression.
48          Protein VII associated with SET and pp32 in vitro and distinct domains of protein VII were r
49 I (PHAPI, also known as the tumor suppressor pp32) in HT29 human colon cancer cells.
50 alization and transfection studies show that pp32 INHAT domains are responsible for histone binding,
51  In contrast, in cotransfection experiments, pp32 inhibited the ability of a broad assortment of onco
52                      In related experiments, pp32 inhibited the ability of Rat 1a-myc cells to grow i
53                                      Because pp32 inhibits oncogene-mediated transformation, we inves
54 mic acid residues; the predicted pI of human pp32 is 3.81.
55                Thus phosphorylation of PHAPI/pp32 is a critical regulatory step in PP2A activation an
56                                              pp32 is a nuclear protein found highly expressed in norm
57                                     Although pp32 is a phosphoprotein, neither the phosphorylation si
58                                        PHAPI/pp32 is a tumor suppressor whose expression is altered i
59                                     Although pp32 is a tumor suppressor, pp32r1 and pp32r2 are tumori
60            The leucine-rich repeat domain of PP32 is composed of five beta-strand-containing repeats
61                          In benign prostate, pp32 is expressed in basal cells but not in terminally d
62                     Here we demonstrate that pp32 is expressed in benign prostatic tissue, but pp32r1
63 r affinity for phospho-pp32 demonstrate that pp32 is indeed phosphorylated in vivo at these two sites
64                 The versatile phosphoprotein pp32 is involved in important physiological processes, i
65 onstrate that the main barrier to folding of pp32 is quite broad and lies near the unfolded state, wi
66                    Although the structure of pp32 is suggestive of a transcription factor, pp32 did n
67                                 However, how pp32 itself is regulated remained largely unknown.
68                    The identification of the pp32 kinase and the sites of pp32 phosphorylation as wel
69 , we identify casein kinase II as a cellular pp32-kinase.
70                   These results suggest that pp32 may play a key role in self-renewing cell populatio
71                             Mechanistically, pp32 may regulate pathways important in the process of d
72 fication of the pp32 kinase and the sites of pp32 phosphorylation as well as the generation of antibo
73                       Alternative use of the pp32, pp32r1 and pp32r2 genes may modulate the oncogenic
74                        At the protein level, pp32, pp32r1, and pp32r2 are approximately 90% identical
75 tic role for the mammalian Set/TAF-Ibeta and pp32 proteins as transducers of chromatin signaling by i
76                  We further demonstrate that pp32-Rb interaction inhibits the apoptotic activity of p
77                                              pp32 reduction induced TSU-Pr1 cells to differentiate in
78  information and tools for future studies on pp32 regulation.
79 onstrate that tumor-suppressive functions of pp32 reside in amino acids 150-174.
80  antibodies with higher affinity for phospho-pp32 should now provide key information and tools for fu
81 er by comparing the sequence and function of pp32 species from paired benign prostate tissue and adja
82 late-activating factor-Ibeta (TAF-Ibeta) and pp32, specifically bind to unacetylated, hypoacetylated,
83 containing the Set/TAF-Ibeta oncoprotein and pp32 strongly inhibits the HAT activity of p300/CBP and
84                       Mutagenesis studies on pp32 suggest a role for serines 158 and 204 in its funct
85 ifferentiated tumors express lower levels of pp32 than poorly differentiated tumors.
86 5K interacting factors, importin-alpha 1 and pp32, that may also participate in the functions previou
87             We have previously reported that pp32, through histone masking, inhibits histone acetylat
88                   Through kinetic studies of PP32, we find folding to be rate-limited by the formatio
89 ing corresponds to the most stable region of PP32, we monitored amide hydrogen exchange by NMR spectr
90                                Comparison of pp32 with the pp32r1 sequence by moving averages of sequ

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