PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32699085-8 2020 Expressing the ZIKV NS5 SUMO site mutant (K252R) resulted in NS5/STAT2/PML NBs that failed to degrade PML, reduce STAT2 expression or inhibit ISG induction. Bromosuccinimide 75-78 PML nuclear body scaffold Homo sapiens 71-74 32243901-7 2020 PML is sumoylated and contains a Sumo-interacting motif, and a significant fraction of Sumo1 and Sumo2/3 co-localizes with PML NBs. Bromosuccinimide 127-130 PML nuclear body scaffold Homo sapiens 123-126 32243901-8 2020 Ectopic expression of the mutant C204A selectively inhibits the biogenesis of endogenous PML NBs but not PML-less Sumo1-, Sumo2/3, or Daxx-containing nuclear speckles. Bromosuccinimide 93-96 PML nuclear body scaffold Homo sapiens 89-92 32154186-13 2020 In contrast, human papillomavirus (HPV) infection requires the presence of PML protein suggesting that PML NBs may be essential to establish infection. Bromosuccinimide 107-110 PML nuclear body scaffold Homo sapiens 75-78 30292834-8 2018 These results indicate that As3+ selectively reorganizes PML and SUMO2/3 monomers into insoluble forms in PML-NBs, and then PML SUMOylation proceeds. Bromosuccinimide 110-113 PML nuclear body scaffold Homo sapiens 106-109 30292834-8 2018 These results indicate that As3+ selectively reorganizes PML and SUMO2/3 monomers into insoluble forms in PML-NBs, and then PML SUMOylation proceeds. Bromosuccinimide 110-113 PML nuclear body scaffold Homo sapiens 106-109 28525371-5 2017 Conversely, knockdown of RNF4 led to a remarkable increase in PML SUMOylation and the function of PML-NBs, further promoting ATO- or Ang II-induced HERG protein downregulation. Bromosuccinimide 102-105 PML nuclear body scaffold Homo sapiens 98-101 28863453-7 2017 These structures were consistently colocalized with promyelocytic leukemia protein (PML), an essential component of NBs, in particular when activated. Bromosuccinimide 116-119 PML nuclear body scaffold Homo sapiens 52-82 28863453-7 2017 These structures were consistently colocalized with promyelocytic leukemia protein (PML), an essential component of NBs, in particular when activated. Bromosuccinimide 116-119 PML nuclear body scaffold Homo sapiens 84-87 27903803-14 2017 In this paper, we further elucidate the molecular mechanism for how IE1 antagonizes PML NBs. Bromosuccinimide 88-91 PML nuclear body scaffold Homo sapiens 84-87 24036361-8 2013 Thus, we report eIF3K as the first known subunit of the eIF3 translation pre-initiation complex to interact directly with the PML protein, and provide data implicating alternative splicing of both PML and eIF3K as a possible regulatory mechanism for eIF3K localization at PML NBs. Bromosuccinimide 276-279 PML nuclear body scaffold Homo sapiens 126-129 24036361-8 2013 Thus, we report eIF3K as the first known subunit of the eIF3 translation pre-initiation complex to interact directly with the PML protein, and provide data implicating alternative splicing of both PML and eIF3K as a possible regulatory mechanism for eIF3K localization at PML NBs. Bromosuccinimide 276-279 PML nuclear body scaffold Homo sapiens 197-200 24036361-8 2013 Thus, we report eIF3K as the first known subunit of the eIF3 translation pre-initiation complex to interact directly with the PML protein, and provide data implicating alternative splicing of both PML and eIF3K as a possible regulatory mechanism for eIF3K localization at PML NBs. Bromosuccinimide 276-279 PML nuclear body scaffold Homo sapiens 197-200 22117195-7 2012 This reduction in PML post-translational modification promotes defects in PML-NBs formation. Bromosuccinimide 78-81 PML nuclear body scaffold Homo sapiens 18-21 22117195-7 2012 This reduction in PML post-translational modification promotes defects in PML-NBs formation. Bromosuccinimide 78-81 PML nuclear body scaffold Homo sapiens 74-77 22033920-6 2011 Consistent with this observation, phosphorylated ERK2 partially co-localized with PML NBs. Bromosuccinimide 86-89 PML nuclear body scaffold Homo sapiens 82-85 22033920-9 2011 In contrast, knockdown of ERK2 by siRNA resulted in an increase in PML protein levels and an increase in the formation of PML NBs. Bromosuccinimide 126-129 PML nuclear body scaffold Homo sapiens 122-125 21217775-9 2011 Furthermore, treatment with arsenic trioxide (ATO) induced PML sumoylation and reconstitution of PML NBs, and overcame the anti-apoptotic effect of PAX5-PML in HeLa cells. Bromosuccinimide 101-104 PML nuclear body scaffold Homo sapiens 97-100 21217775-9 2011 Furthermore, treatment with arsenic trioxide (ATO) induced PML sumoylation and reconstitution of PML NBs, and overcame the anti-apoptotic effect of PAX5-PML in HeLa cells. Bromosuccinimide 101-104 PML nuclear body scaffold Homo sapiens 97-100 21198351-5 2011 Accumulating reports have implicated PML in host antiviral defense and revealed various strategies developed by viruses to disrupt PML NBs. Bromosuccinimide 135-138 PML nuclear body scaffold Homo sapiens 131-134 20826694-4 2010 RNA viruses whose replication takes place in the cytoplasm and is inhibited by PML have developed various strategies to counteract the antiviral defense mediated by PML NBs. Bromosuccinimide 169-172 PML nuclear body scaffold Homo sapiens 79-82 20826694-4 2010 RNA viruses whose replication takes place in the cytoplasm and is inhibited by PML have developed various strategies to counteract the antiviral defense mediated by PML NBs. Bromosuccinimide 169-172 PML nuclear body scaffold Homo sapiens 165-168 20702643-2 2010 PML conjugation to the small ubiquitin-like modifier (SUMO) is required for its localization within NBs. Bromosuccinimide 100-103 PML nuclear body scaffold Homo sapiens 0-3 18625722-3 2008 Here, we show that histone deacetylase 7 (HDAC7) knockdown reduces the size and the number of the PML NBs in human umbilical vein endothelial cells (HUVECs). Bromosuccinimide 102-105 PML nuclear body scaffold Homo sapiens 98-101 18625722-6 2008 Importantly, HDAC7 knockdown inhibits tumor necrosis factor alpha-induced PML sumoylation and the formation of PML NBs in HUVECs. Bromosuccinimide 115-118 PML nuclear body scaffold Homo sapiens 111-114 18664490-9 2008 DAXX and BLM turn over rapidly and completely at PML NBs within seconds. Bromosuccinimide 53-56 PML nuclear body scaffold Homo sapiens 49-52 18463162-3 2008 We show here that endogenous HDAC7 and PML interact and partially colocalize in PML NBs. Bromosuccinimide 84-87 PML nuclear body scaffold Homo sapiens 39-42 18463162-3 2008 We show here that endogenous HDAC7 and PML interact and partially colocalize in PML NBs. Bromosuccinimide 84-87 PML nuclear body scaffold Homo sapiens 80-83 18463162-7 2008 Accordingly, ectopic expression of PML recruits HDAC7 to PML NBs and leads to activation of MEF2 reporter activity. Bromosuccinimide 61-64 PML nuclear body scaffold Homo sapiens 35-38 18463162-7 2008 Accordingly, ectopic expression of PML recruits HDAC7 to PML NBs and leads to activation of MEF2 reporter activity. Bromosuccinimide 61-64 PML nuclear body scaffold Homo sapiens 57-60 17343971-8 2007 Although there are many other functions of PML NBs in a wide range of cellular pathways, there is accumulating evidence that they represent preferential targets for viral infections and that PML plays a role in the mechanism of the antiviral action of IFN. Bromosuccinimide 47-50 PML nuclear body scaffold Homo sapiens 43-46 16117725-7 2005 Concomitantly the number of nuclear ubiquitin clusters decreased, and were almost quantitatively associated with the PML NBs, co-localizing with the SUMO-conjugated pool. Bromosuccinimide 121-124 PML nuclear body scaffold Homo sapiens 117-120 15459016-9 2005 Identification of PML and PML NBs as effectors of IFN responses provides insights into mechanisms by which tumor cells exhibit resistance to this class of agents and may prove useful in assessing treatment regimens. Bromosuccinimide 30-33 PML nuclear body scaffold Homo sapiens 26-29 14712236-5 2004 Similar to the dispersal of PML NBs in response to some viral infections, PML redistribution after DNA damage was inhibited by the proteasome inhibitor MG132. Bromosuccinimide 32-35 PML nuclear body scaffold Homo sapiens 28-31 14712236-5 2004 Similar to the dispersal of PML NBs in response to some viral infections, PML redistribution after DNA damage was inhibited by the proteasome inhibitor MG132. Bromosuccinimide 32-35 PML nuclear body scaffold Homo sapiens 74-77 12077003-10 2002 CREB-binding protein (CBP), another component of NBs, was distributed like PML in NIIs. Bromosuccinimide 49-52 PML nuclear body scaffold Homo sapiens 75-78 11704856-5 2001 Modification of PML by the Small Ubiquitin MOdifier (SUMO) was shown to be required for its localization in NBs. Bromosuccinimide 108-111 PML nuclear body scaffold Homo sapiens 16-19 11413191-2 2001 In acute promyelocytic leukemia, PML/retinoic acid receptor (RAR) alpha expression disrupts NBs, but therapies such as retinoic acid or arsenic trioxide (As2O3) restore them. Bromosuccinimide 92-95 PML nuclear body scaffold Homo sapiens 33-36 11413191-5 2001 PML sumolation is dispensable for its As2O3-induced matrix targeting and formation of primary nuclear aggregates, but is required for the formation of secondary shell-like NBs. Bromosuccinimide 172-175 PML nuclear body scaffold Homo sapiens 0-3 9294197-3 1997 Furthermore, induction of PML expression by interferons leads to a recruitment of PLZF onto NBs without increase in the levels of the PLZF protein. Bromosuccinimide 92-95 PML nuclear body scaffold Homo sapiens 26-29 35594310-4 2022 However, topological changes of PML-NBs in As3+-exposed cells have not been well-documented. Bromosuccinimide 36-39 PML nuclear body scaffold Homo sapiens 32-35 35594310-5 2022 We report that As3+-induced solubility shift underlies rapid SUMOylation of PML and late agglomeration of PML-NBs. Bromosuccinimide 110-113 PML nuclear body scaffold Homo sapiens 106-109 35594310-11 2022 These results warrant the importance of As3+- or Sb3+-induced solubility shift of PML for the regulation intranuclear dynamics of PML-NBs. Bromosuccinimide 134-137 PML nuclear body scaffold Homo sapiens 82-85 35594310-11 2022 These results warrant the importance of As3+- or Sb3+-induced solubility shift of PML for the regulation intranuclear dynamics of PML-NBs. Bromosuccinimide 134-137 PML nuclear body scaffold Homo sapiens 130-133 35194189-2 2022 PML NBs are critical to tumor suppression, and their disruption mediated by PML/RARalpha accelerates APL pathogenesis. Bromosuccinimide 4-7 PML nuclear body scaffold Homo sapiens 76-79 35194189-6 2022 Accordingly, deneddylation of PML/RARalpha restores its phase separation process to reconstruct functional NBs and activates RARalpha signaling, thereby suppressing PML/RARalpha-driven leukemogenesis. Bromosuccinimide 107-110 PML nuclear body scaffold Homo sapiens 30-33 35194189-6 2022 Accordingly, deneddylation of PML/RARalpha restores its phase separation process to reconstruct functional NBs and activates RARalpha signaling, thereby suppressing PML/RARalpha-driven leukemogenesis. Bromosuccinimide 107-110 PML nuclear body scaffold Homo sapiens 165-168