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Statements

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n5:pmcid: PMC0
bibo:doi: 10.1371%2Fjournal.pone.0025370
n4:contains: _:vb12812207 _:vb12812235 _:vb12812249

Subject Item: _:vb12812207
rdf:type: n4:Section
dc:title: introduction
n4:contains: _:vb12812233 _:vb12812234 _:vb12812224 _:vb12812225 _:vb12812226 _:vb12812227 _:vb12812228 _:vb12812229 _:vb12812230 _:vb12812231 _:vb12812216 _:vb12812217 _:vb12812218 _:vb12812219 _:vb12812220 _:vb12812221 _:vb12812222 _:vb12812223 _:vb12812208 _:vb12812209 _:vb12812210 _:vb12812211 _:vb12812212 _:vb12812213 _:vb12812214 _:vb12812215 _:vb12812232

Subject Item: _:vb12812208
rdf:type: n5:Context
rdf:value: One of the genes associated with both murine and human myeloid leukemia is EVI1 [>>1<<], [2]. Over expression and aberrant expression of EVI1 was shown to be associated with most forms of human leukemia, as a consequence of chromosomal rearrangements involving 3q26.2, where the gene is mapped [3] and also without
n5:mentions: n2:2842066

Subject Item: _:vb12812209
rdf:type: n5:Context
rdf:value: One of the genes associated with both murine and human myeloid leukemia is EVI1 [1], [>>2<<]. Over expression and aberrant expression of EVI1 was shown to be associated with most forms of human leukemia, as a consequence of chromosomal rearrangements involving 3q26.2, where the gene is mapped [3] and also without cytogenetically
n5:mentions: n2:8656673

Subject Item: _:vb12812210
rdf:type: n5:Context
rdf:value: Over expression and aberrant expression of EVI1 was shown to be associated with most forms of human leukemia, as a consequence of chromosomal rearrangements involving 3q26.2, where the gene is mapped [>>3<<] and also without cytogenetically detectable rearrangements of the EVI1 locus as a result of unknown mechanism [2], [4].
n5:mentions: n2:17507183

Subject Item: _:vb12812211
rdf:type: n5:Context
rdf:value: most forms of human leukemia, as a consequence of chromosomal rearrangements involving 3q26.2, where the gene is mapped [3] and also without cytogenetically detectable rearrangements of the EVI1 locus as a result of unknown mechanism [>>2<<], [4]. Overall up regulation of EVI1 has been shown in 30% of advanced CML patients, 8–10% of MDS –AML patients and 7.8% of de novo AML cases [5]–[7].
n5:mentions: n2:8656673

Subject Item: _:vb12812212
rdf:type: n5:Context
rdf:value: forms of human leukemia, as a consequence of chromosomal rearrangements involving 3q26.2, where the gene is mapped [3] and also without cytogenetically detectable rearrangements of the EVI1 locus as a result of unknown mechanism [2], [>>4<<]. Overall up regulation of EVI1 has been shown in 30% of advanced CML patients, 8–10% of MDS –AML patients and 7.8% of de novo AML cases [5]–[7].
n5:mentions: n2:8049440

Subject Item: _:vb12812213
rdf:type: n5:Context
rdf:value: Overall up regulation of EVI1 has been shown in 30% of advanced CML patients, 8–10% of MDS –AML patients and 7.8% of de novo AML cases [>>5<<]–[7]. Also studies indicate that EVI1 may be over expressed in a subset of human colon cancers, and that EVI1 might affect disease progression and/or sensitivity to chemotherapy [8]. The protein is highly conserved through evolution and
n5:mentions: n2:7780155

Subject Item: _:vb12812214
rdf:type: n5:Context
rdf:value: Overall up regulation of EVI1 has been shown in 30% of advanced CML patients, 8–10% of MDS –AML patients and 7.8% of de novo AML cases [5]–[>>7<<]. Also studies indicate that EVI1 may be over expressed in a subset of human colon cancers, and that EVI1 might affect disease progression and/or sensitivity to chemotherapy [8]. The protein is highly conserved through evolution and
n5:mentions: n2:18272813

Subject Item: _:vb12812215
rdf:type: n5:Context
rdf:value: Also studies indicate that EVI1 may be over expressed in a subset of human colon cancers, and that EVI1 might affect disease progression and/or sensitivity to chemotherapy [>>8<<]. The protein is highly conserved through evolution and encodes a repressor and an activator domain with two sets of zinc finger motifs [1], [3], [9], [10]. Both zinc finger domains of EVI1 recognize and bind to specific DNA consensus
n5:mentions: n2:16462766

Subject Item: _:vb12812216
rdf:type: n5:Context
rdf:value: The protein is highly conserved through evolution and encodes a repressor and an activator domain with two sets of zinc finger motifs [>>1<<], [3], [9], [10].
n5:mentions: n2:2842066

Subject Item: _:vb12812217
rdf:type: n5:Context
rdf:value: The protein is highly conserved through evolution and encodes a repressor and an activator domain with two sets of zinc finger motifs [1], [>>3<<], [9], [10].
n5:mentions: n2:17507183

Subject Item: _:vb12812218
rdf:type: n5:Context
rdf:value: The protein is highly conserved through evolution and encodes a repressor and an activator domain with two sets of zinc finger motifs [1], [3], [>>9<<], [10]. Both zinc finger domains of EVI1 recognize and bind to specific DNA consensus sequence in vitro and in vivo, of which some are characterized and some are not functionally characterized [3], [11], [12]. Some known functionally
n5:mentions: n2:2115646

Subject Item: _:vb12812219
rdf:type: n5:Context
rdf:value: The protein is highly conserved through evolution and encodes a repressor and an activator domain with two sets of zinc finger motifs [1], [3], [9], [>>10<<]. Both zinc finger domains of EVI1 recognize and bind to specific DNA consensus sequence in vitro and in vivo, of which some are characterized and some are not functionally characterized [3], [11], [12]. Some known functionally relevant
n5:mentions: n2:8108138

Subject Item: _:vb12812220
rdf:type: n5:Context
rdf:value: Both zinc finger domains of EVI1 recognize and bind to specific DNA consensus sequence in vitro and in vivo, of which some are characterized and some are not functionally characterized [>>3<<], [11], [12].
n5:mentions: n2:17507183

Subject Item: _:vb12812221
rdf:type: n5:Context
rdf:value: Both zinc finger domains of EVI1 recognize and bind to specific DNA consensus sequence in vitro and in vivo, of which some are characterized and some are not functionally characterized [3], [>>11<<], [12]. Some known functionally relevant targets of EVI1 includes Pbx1, calreticulin and GATA2 which are involved in calcium metabolism, maintenance of adequate number of hematopoietic stem cells and self renewal of hematopoietic stem
n5:mentions: n2:19767769

Subject Item: _:vb12812222
rdf:type: n5:Context
rdf:value: Both zinc finger domains of EVI1 recognize and bind to specific DNA consensus sequence in vitro and in vivo, of which some are characterized and some are not functionally characterized [3], [11], [>>12<<]. Some known functionally relevant targets of EVI1 includes Pbx1, calreticulin and GATA2 which are involved in calcium metabolism, maintenance of adequate number of hematopoietic stem cells and self renewal of hematopoietic stem cells
n5:mentions: n2:20015077

Subject Item: _:vb12812223
rdf:type: n5:Context
rdf:value: Some known functionally relevant targets of EVI1 includes Pbx1, calreticulin and GATA2 which are involved in calcium metabolism, maintenance of adequate number of hematopoietic stem cells and self renewal of hematopoietic stem cells [>>11<<], [13], [14]. However, the exact mechanism by which EVI1 promotes cell proliferation and blocks apoptosis still remains unclear.
n5:mentions: n2:19767769

Subject Item: _:vb12812224
rdf:type: n5:Context
rdf:value: known functionally relevant targets of EVI1 includes Pbx1, calreticulin and GATA2 which are involved in calcium metabolism, maintenance of adequate number of hematopoietic stem cells and self renewal of hematopoietic stem cells [11], [>>13<<], [14]. However, the exact mechanism by which EVI1 promotes cell proliferation and blocks apoptosis still remains unclear.
n5:mentions: n2:18303859

Subject Item: _:vb12812225
rdf:type: n5:Context
rdf:value: functionally relevant targets of EVI1 includes Pbx1, calreticulin and GATA2 which are involved in calcium metabolism, maintenance of adequate number of hematopoietic stem cells and self renewal of hematopoietic stem cells [11], [13], [>>14<<]. However, the exact mechanism by which EVI1 promotes cell proliferation and blocks apoptosis still remains unclear.
n5:mentions: n2:15889140

Subject Item: _:vb12812226
rdf:type: n5:Context
rdf:value: Apoptosis is a critical process that is deregulated in oncogenesis [>>15<<]. Bcl-2 and Bcl-xL are anti-apoptotic paralogues that inhibit apoptosis which is elicited by a wide variety of stimuli, and play critical roles in cancer development and resistance to treatment whereas BAD, BAX, BID and PUMA enhance DNA
n5:mentions: n2:10647931

Subject Item: _:vb12812227
rdf:type: n5:Context
rdf:value: paralogues that inhibit apoptosis which is elicited by a wide variety of stimuli, and play critical roles in cancer development and resistance to treatment whereas BAD, BAX, BID and PUMA enhance DNA damage induced apoptosis [>>16<<]. Subtle changes in the cellular levels of Bcl-xL expression can have dramatic phenotypes.
n5:mentions: n2:12209154

Subject Item: _:vb12812228
rdf:type: n5:Context
rdf:value: Recently it was shown that HIF-1α can directly up regulate Bcl-xL gene transcription and can protect prostate cancer cells from apoptosis [>>17<<]. Inducible expression of EVI1 or MDS1/EVI1 in the human myelomonocytic cell line U937T lead to cell cycle arrest and massive apoptosis upon exposure to differentiation stimuli, thereby recapitulating salient aspects of the biology of MDS
n5:mentions: n2:19211554

Subject Item: _:vb12812229
rdf:type: n5:Context
rdf:value: of EVI1 or MDS1/EVI1 in the human myelomonocytic cell line U937T lead to cell cycle arrest and massive apoptosis upon exposure to differentiation stimuli, thereby recapitulating salient aspects of the biology of MDS in vitro [>>18<<]. EVI1 activates PI3K/AKT signaling and suppresses TGF-β mediated apoptosis [8].
n5:mentions: n2:19605700

Subject Item: _:vb12812230
rdf:type: n5:Context
rdf:value: EVI1 activates PI3K/AKT signaling and suppresses TGF-β mediated apoptosis [>>8<<]. This property of EVI1 appears likely to be integral to its oncogenic potential, since loss of response to apoptotic signals is one of the signs of transformation.
n5:mentions: n2:16462766

Subject Item: _:vb12812231
rdf:type: n5:Context
rdf:value: It was shown earlier that interaction of EVI1 with different co-regulators could result in periodic, reversible acetylation and deacetylation of EVI1 and assembly of acetylated EVI1 in nuclear speckles [>>19<<]. The nuclear speckles are associated with cellular functions such as DNA replication, gene transcription and regulation of apoptosis. Evasion of apoptosis has been observed in both EVI1 positive hematopoietic and epithelial cells and
n5:mentions: n2:11568182

Subject Item: _:vb12812232
rdf:type: n5:Context
rdf:value: Evasion of apoptosis has been observed in both EVI1 positive hematopoietic and epithelial cells and suggests that EVI1 is a survival factor [>>8<<], [20], [21], however none of them are mutually exclusive and additional mechanisms mediating the survival promoting effects of EVI1 may also exist.
n5:mentions: n2:16462766

Subject Item: _:vb12812233
rdf:type: n5:Context
rdf:value: Evasion of apoptosis has been observed in both EVI1 positive hematopoietic and epithelial cells and suggests that EVI1 is a survival factor [8], [>>20<<], [21], however none of them are mutually exclusive and additional mechanisms mediating the survival promoting effects of EVI1 may also exist.
n5:mentions: n2:15343390

Subject Item: _:vb12812234
rdf:type: n5:Context
rdf:value: Evasion of apoptosis has been observed in both EVI1 positive hematopoietic and epithelial cells and suggests that EVI1 is a survival factor [8], [20], [>>21<<], however none of them are mutually exclusive and additional mechanisms mediating the survival promoting effects of EVI1 may also exist.
n5:mentions: n2:10856240

Subject Item: _:vb12812235
rdf:type: n4:Section
dc:title: results
n4:contains: _:vb12812236 _:vb12812237 _:vb12812238 _:vb12812239 _:vb12812248 _:vb12812240 _:vb12812241 _:vb12812242 _:vb12812243 _:vb12812244 _:vb12812245 _:vb12812246 _:vb12812247

Subject Item: _:vb12812236
rdf:type: n5:Context
rdf:value: Most interestingly the same region was previously shown to be a target of GATA1 and EVI1 by computational analysis in mouse Bcl-xL promoter [>>22<<]. Studies have shown earlier that the homology between rat, mouse and human Bcl-xL gene is extremely high across the region encompassing exons 1B through to exon 3 [23]. We also found that the identified region is almost conserved across
n5:mentions: n2:9144489

Subject Item: _:vb12812237
rdf:type: n5:Context
rdf:value: Studies have shown earlier that the homology between rat, mouse and human Bcl-xL gene is extremely high across the region encompassing exons 1B through to exon 3 [>>23<<]. We also found that the identified region is almost conserved across species (Figure 1A). This finding suggests that Bcl-xL could be a direct transcriptional target of EVI1 which is conserved among species. To examine if EVI1 can bind to
n5:mentions: n2:12721309

Subject Item: _:vb12812238
rdf:type: n5:Context
rdf:value: Bioinformatics analysis has earlier shown that the same site is also occupied by the GATA1 transcription factor [>>22<<]. The role of GATA1 in Bcl-xL expression has been obscure because mutations in the typical GATA binding site did not affect GATA1 activated Bcl-xL transcription [24]. However contrasting report states that GATA1 binds to the GATT motif
n5:mentions: n2:9144489

Subject Item: _:vb12812239
rdf:type: n5:Context
rdf:value: The role of GATA1 in Bcl-xL expression has been obscure because mutations in the typical GATA binding site did not affect GATA1 activated Bcl-xL transcription [>>24<<]. However contrasting report states that GATA1 binds to the GATT motif (404 bp or 408 bp upstream of the translation start site in mouse and human Bcl-xL promoters) and mutation of the site shows deregulation of Bcl-xL function [25]. As
n5:mentions: n2:10381501

Subject Item: _:vb12812240
rdf:type: n5:Context
rdf:value: However contrasting report states that GATA1 binds to the GATT motif (404 bp or 408 bp upstream of the translation start site in mouse and human Bcl-xL promoters) and mutation of the site shows deregulation of Bcl-xL function [>>25<<]. As mutation in the GATA1 binding site (408 bp upstream of the translation start site) down regulates Bcl-xL so the bioinformatically gathered GATA1 site [22] 113 bp upstream of the translation start site may not be active. It is possible
n5:mentions: n2:17420275

Subject Item: _:vb12812241
rdf:type: n5:Context
rdf:value: As mutation in the GATA1 binding site (408 bp upstream of the translation start site) down regulates Bcl-xL so the bioinformatically gathered GATA1 site [>>22<<] 113 bp upstream of the translation start site may not be active.
n5:mentions: n2:9144489

Subject Item: _:vb12812242
rdf:type: n5:Context
rdf:value: that EVI1 directly binds to the region 113 bp upstream of the start codon and GATA1 binds to EVI1 at this site to give a delayed kinetics of Bcl-xL induction as it has been shown that both the proteins interact with each other [>>26<<]. Again to rule out the possibility that GATA1 binds to the same region we also used NIH 3T3 cells which lack GATA1 to show that EVI1 can directly up regulate Bcl-xL promoter activity (Figure 2F).
n5:mentions: n2:16954386

Subject Item: _:vb12812243
rdf:type: n5:Context
rdf:value: Earlier we have shown that the proto-oncogene EVI1 was acetylated in vivo [>>19<<]. Since studies have shown that reversible acetylation of EVI1 are associated with nuclear speckles and nuclear speckles are known to be associated with different cellular functions including apoptosis we wanted to know if acetylated EVI1
n5:mentions: n2:11568182

Subject Item: _:vb12812244
rdf:type: n5:Context
rdf:value: Unlike the previous work where acetylated EVI1 activated the synthetic promoter [>>19<<] here we found that PCAF acetylated EVI1 reduced Bcl-xL transcriptional activity with respect to wild type EVI1 in 293T cells (Figure 3C).
n5:mentions: n2:11568182

Subject Item: _:vb12812245
rdf:type: n5:Context
rdf:value: EVI1 blocks cell death by selectively binding and inhibiting JNK and also EVI1 specifically represses the IFN-dependent induction of the tumor suppressor PML and blocks the apoptotic pathway activated by PML [>>21<<], [27]. In addition to the ability to inhibit Smad-mediated signaling, EVI1 also functions as a survival gene by activating an anti-apoptotic P13K/AKT signaling pathway in both non-transformed intestinal epithelial cells and in colon
n5:mentions: n2:10856240

Subject Item: _:vb12812246
rdf:type: n5:Context
rdf:value: EVI1 blocks cell death by selectively binding and inhibiting JNK and also EVI1 specifically represses the IFN-dependent induction of the tumor suppressor PML and blocks the apoptotic pathway activated by PML [21], [>>27<<]. In addition to the ability to inhibit Smad-mediated signaling, EVI1 also functions as a survival gene by activating an anti-apoptotic P13K/AKT signaling pathway in both non-transformed intestinal epithelial cells and in colon cancer
n5:mentions: n2:15519999

Subject Item: _:vb12812247
rdf:type: n5:Context
rdf:value: Earlier apoptosis assay was shown in HT-29 cells by using taxol [>>8<<], however we have used plumbagin as plumbagin has no effect on PCAF mediated acetylation in vivo [28].
n5:mentions: n2:16462766

Subject Item: _:vb12812248
rdf:type: n5:Context
rdf:value: Earlier apoptosis assay was shown in HT-29 cells by using taxol [8], however we have used plumbagin as plumbagin has no effect on PCAF mediated acetylation in vivo [>>28<<]. EVI1 siRNA was used for a set of cells to down regulate the expression of EVI1. Cells were treated in duplicate with plumbagin for 12 h in culture and then assayed for apoptosis using the Annexin-V-PE & 7-AAD apoptosis detection kit.
n5:mentions: n2:19570987

Subject Item: _:vb12812249
rdf:type: n4:Section
dc:title: discussion
n4:contains: _:vb12812250 _:vb12812251 _:vb12812252 _:vb12812253 _:vb12812254 _:vb12812255 _:vb12812256 _:vb12812257 _:vb12812258 _:vb12812259 _:vb12812260 _:vb12812261 _:vb12812262 _:vb12812263 _:vb12812264 _:vb12812265

Subject Item: _:vb12812250
rdf:type: n5:Context
rdf:value: Apoptosis, triggered by a variety of intra- and extra cellular signals, is important for normal development, to maintain tissue homeostasis, and as a defense strategy against the emergence of cancer [>>29<<], [30]. However, alterations in the relative level of intracellular pro- versus anti-apoptotic Bcl-2 family proteins are implicated in tumorigenesis in both clinical cases and transgenic models [31].
n5:mentions: n2:10561374

Subject Item: _:vb12812251
rdf:type: n5:Context
rdf:value: Apoptosis, triggered by a variety of intra- and extra cellular signals, is important for normal development, to maintain tissue homeostasis, and as a defense strategy against the emergence of cancer [29], [>>30<<]. However, alterations in the relative level of intracellular pro- versus anti-apoptotic Bcl-2 family proteins are implicated in tumorigenesis in both clinical cases and transgenic models [31].
n5:mentions: n2:1557121

Subject Item: _:vb12812252
rdf:type: n5:Context
rdf:value: However, alterations in the relative level of intracellular pro- versus anti-apoptotic Bcl-2 family proteins are implicated in tumorigenesis in both clinical cases and transgenic models [>>31<<]. Clinical studies that demonstrated increased level of Bcl-xL in breast carcinoma, gastric cancer cells and others are associated with a poor outcome. In addition, these members are also important determinants of anticancer drug
n5:mentions: n2:9721090

Subject Item: _:vb12812253
rdf:type: n5:Context
rdf:value: In addition, these members are also important determinants of anticancer drug sensitivity [>>32<<]. We found that the proto-oncogene EVI1 not only binds Bcl-xL promoter but also up regulates its transcriptional activity and protein expression. We confirmed the occupancy of this site by EVI1 using ChIP analysis in HT-29/293T cells and
n5:mentions: n2:11085534

Subject Item: _:vb12812254
rdf:type: n5:Context
rdf:value: Bcl-xL on the other hand is regulated by several other transcription factor families, including STATs (signal transducers and activators of transcription) [>>33<<], NF-κB [34], Ets [35], GATA [24], and HIF-1α [17], suggesting that Bcl-xL is induced by different transcription mechanisms depending on the cellular context and the stimulated signals.
n5:mentions: n2:9185513

Subject Item: _:vb12812255
rdf:type: n5:Context
rdf:value: Bcl-xL on the other hand is regulated by several other transcription factor families, including STATs (signal transducers and activators of transcription) [33], NF-κB [>>34<<], Ets [35], GATA [24], and HIF-1α [17], suggesting that Bcl-xL is induced by different transcription mechanisms depending on the cellular context and the stimulated signals.
n5:mentions: n2:10733571

Subject Item: _:vb12812256
rdf:type: n5:Context
rdf:value: Bcl-xL on the other hand is regulated by several other transcription factor families, including STATs (signal transducers and activators of transcription) [33], NF-κB [34], Ets [>>35<<], GATA [24], and HIF-1α [17], suggesting that Bcl-xL is induced by different transcription mechanisms depending on the cellular context and the stimulated signals.
n5:mentions: n2:10082528

Subject Item: _:vb12812257
rdf:type: n5:Context
rdf:value: Bcl-xL on the other hand is regulated by several other transcription factor families, including STATs (signal transducers and activators of transcription) [33], NF-κB [34], Ets [35], GATA [>>24<<], and HIF-1α [17], suggesting that Bcl-xL is induced by different transcription mechanisms depending on the cellular context and the stimulated signals.
n5:mentions: n2:10381501

Subject Item: _:vb12812258
rdf:type: n5:Context
rdf:value: Bcl-xL on the other hand is regulated by several other transcription factor families, including STATs (signal transducers and activators of transcription) [33], NF-κB [34], Ets [35], GATA [24], and HIF-1α [>>17<<], suggesting that Bcl-xL is induced by different transcription mechanisms depending on the cellular context and the stimulated signals.
n5:mentions: n2:19211554

Subject Item: _:vb12812259
rdf:type: n5:Context
rdf:value: Cells over expressing Bcl-xL mediated by an oncogene can help in the cell survival following DNA damage and can potentially accumulate new somatic mutations at higher frequencies [>>36<<]. It was reported earlier that activation of STAT5 can contribute to Bcl-X induction in CML; however STAT5 by itself is not sufficient. Other pathways including activation through IL-3 receptor or PI-3K has also been reported. Thus in an
n5:mentions: n2:8875987

Subject Item: _:vb12812260
rdf:type: n5:Context
rdf:value: the ability of Ku70 to suppress Bax-mediated apoptosis, demonstrating that acetylation negatively regulates the antiapoptotic function of Ku70 in vivo, thus providing a critical link between acetyltransferase and tumor suppression [>>37<<]. On a separate note, acetylation of FoxO1 activates Bim expression to induce apoptosis in response to HDAC inhibitor depsipeptide [38], but FoxO3 induced expression of the cell death gene BIM was not inhibited by treatment of cells with
n5:mentions: n2:15023334

Subject Item: _:vb12812261
rdf:type: n5:Context
rdf:value: On a separate note, acetylation of FoxO1 activates Bim expression to induce apoptosis in response to HDAC inhibitor depsipeptide [>>38<<], but FoxO3 induced expression of the cell death gene BIM was not inhibited by treatment of cells with nicotinamide and TSA [39].
n5:mentions: n2:19308286

Subject Item: _:vb12812262
rdf:type: n5:Context
rdf:value: of FoxO1 activates Bim expression to induce apoptosis in response to HDAC inhibitor depsipeptide [38], but FoxO3 induced expression of the cell death gene BIM was not inhibited by treatment of cells with nicotinamide and TSA [>>39<<]. MYST family mediated acetylation deficient p53 fails to induce apoptosis but not cell cycle arrest as it can selectively block the transcription of proapoptotic target genes such as BAX and PUMA while the nonapoptotic targets p21 and
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Subject Item: _:vb12812263
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rdf:value: deficient p53 fails to induce apoptosis but not cell cycle arrest as it can selectively block the transcription of proapoptotic target genes such as BAX and PUMA while the nonapoptotic targets p21 and hMDM2 remain unaffected [>>40<<]. Any deregulation of acetylation/deacetylation equilibrium or inappropriate modifications could lead to different diseases.
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Subject Item: _:vb12812264
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rdf:value: The sequence-specific DNA binding activity of EVI1 was shown to be dramatically affected by acetylation like in HSF1 and IRF7 [>>41<<], [42], possibly as a result of an acetylation induced change in charge.
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Subject Item: _:vb12812265
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rdf:value: The sequence-specific DNA binding activity of EVI1 was shown to be dramatically affected by acetylation like in HSF1 and IRF7 [41], [>>42<<], possibly as a result of an acetylation induced change in charge.
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