References of "Bours, Vincent"
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See detailActualités thérapeutiques dans le traitement du cancer colorectal
Jerusalem, Guy ULg; Bours, Vincent ULg; Fillet, Georges ULg

in Médecine et Hygiène (1999), 57

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See detailCBP and histone deacetylase inhibition enhance the transactivation potential of the HOXB7 homeodomain-containing protein
Chariot, Alain ULg; Van Lint, Carine; Chapelier, Muriel et al

in Oncogene (1999), 18

Homeodomain-containing proteins are transcription factors regulating the coordinated expression of multiple target genes involved in development, differentiation and cellular transformation. In this study ... [more ▼]

Homeodomain-containing proteins are transcription factors regulating the coordinated expression of multiple target genes involved in development, differentiation and cellular transformation. In this study, we demonstrated that HOXB7, one member of this family, behaved as a transactivator in breast cancer cells. Deletion of either the HOXB7 N-terminal domain or the C-terminal acidic tail abolished this transcriptional effect, suggesting a combination of distinct functional transactivating domains. HOXB7 physically interacted both in vitro and in vivo with the coactivator CREB-binding protein (CBP). This interaction led to an enhanced transactivating potential and required the N-terminal of HOXB7 as well as two domains located at the C-terminal part of CBP. Moreover, trichostatin A, a deacetylase inhibitor, strongly enhanced the transcriptional properties of HOXB7. Our data therefore indicate that HOX proteins can directly interact with CBP and that acetylation/deacetylation may regulate their transcriptional properties. [less ▲]

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See detailSustained NF-kB activity after removal of the etiologic agent in an animal model of asthma
Bureau, Fabrice ULg; Bonizzi, G.; Kirschvink, Nathalie et al

in Proceedings: 1999 International Conference of the American Thoracic Society (1999)

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See detailRepeated Cycles of Retrovirus-Mediated Hsvtk Gene Transfer Plus Ganciclovir Increase Survival of Rats with Peritoneal Carcinomatosis
Princen, Frédéric; Lechanteur, Chantal ULg; Lopez Y Cadenas, Miguel ULg et al

in Gene Therapy (1998), 5(8), 1054-60

Peritoneal carcinomatosis is a common clinical situation that requires novel therapeutic approaches. We investigated the efficiency of an HSVtk gene therapy for the treatment of peritoneal carcinomatosis ... [more ▼]

Peritoneal carcinomatosis is a common clinical situation that requires novel therapeutic approaches. We investigated the efficiency of an HSVtk gene therapy for the treatment of peritoneal carcinomatosis induced in syngeneic rats by DHD/K12 colon carcinoma cells. In this setting, the efficiency of two different retrovirus producing cell lines (GP+AmEnv12 and FLYA13) was compared. Rats treated with a single injection of retrovirus producing cells followed by a 5-day course of ganciclovir treatment showed an increased survival as compared with control animals. Animals treated with three injections of producing cells, each followed by a 4-5-day course of ganciclovir treatment, showed an increased survival as compared with control rats and with those treated with a single cycle of retrovirus producing cells plus ganciclovir. However, only a few animals remained tumor-free after day 180. There was no difference between the two producing cell lines in any of the experiments. RT-PCR demonstrated a faint expression of the tk transgene in the liver, spleen, epiploon, bowels and the lung of the animals injected with the HSVtk producing cells, reflecting most likely the transduction of only a limited number of cells. [less ▲]

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See detailPharma-clinics. Comment je traite... II. Approche thérapeutique du cancer colorectal métastatique
Jerusalem, Guy ULg; Bours, Vincent ULg; Fillet, Georges ULg

in Revue Médicale de Liège (1998), 53(6), 318-21

Since its introduction in 1953, 5-fluorouracil based chemotherapy remained the standard treatment in advanced colorectal cancer. Continuous infusion or biochemical modulation by folinic acid enhanced the ... [more ▼]

Since its introduction in 1953, 5-fluorouracil based chemotherapy remained the standard treatment in advanced colorectal cancer. Continuous infusion or biochemical modulation by folinic acid enhanced the therapeutic efficacy of this agent. Quality of life is limited by the toxicity of these regimens as well as by the frequent visits to the hospital during each cycle. Raltitrexed, a thymidylate synthase inhibitor, offers similar antitumoral activity together with a tolerability in comparison to standard 5-fluorouracil based chemotherapy and its simple dosage schedule also contributes to better quality of life. New chemotherapeutic agents are currently in development for the treatment of patients refractory to 5-fluorouracil. Irinotecan and oxaliplatin demonstrate promising activity. [less ▲]

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See detailActivation of the human immunodeficiency virus long terminal repeat by varicella-zoster virus IE4 protein requires nuclear factor-kB and involves both the amino-terminal and the carboxyl-terminal cysteine-rich region
Defechereux-Thibaut de Maisières, Patricia; Baudoux-Tebache, Laurence; Merville, Marie-Paule ULg et al

in Journal of Biological Chemistry (1998), 273(22), 13636-13644

Varicella-zoster virus open reading frame 4-encoded protein (IE4) possesses transactivating properties for varicella-zoster virus genes as well as for those of heterologous viruses such as the human ... [more ▼]

Varicella-zoster virus open reading frame 4-encoded protein (IE4) possesses transactivating properties for varicella-zoster virus genes as well as for those of heterologous viruses such as the human immunodeficiency virus type 1 (HIV-1). Mechanisms of HIV-1 LTR (long terminal repeat) transactivation were investigated in HeLa cells transiently transfected with an IE4 expression plasmid and a CAT reporter gene under the control of the HIV-1 LTR. These results demonstrated that IE4-mediated transactivation of the HIV-1 LTR in HeLa cells required transcription factor kappaB (NF-kappaB). Using the gel retardation assay, it was shown that transfection of the IE4 expression vector in HeLa cells was not associated with induction of NF-kappaB under the p50.p65 heterodimeric form and that no direct binding of IE4 to the kappaB sites could be detected. Both Western blot and immunofluorescence analyses suggested that the ability of IE4 to activate transcription through kappaB motives was not connected with its capacity to override the inhibitory activities of IkappaB-alpha or p105. Finally, in vitro protein-protein interactions involving IE4 and basal transcription factors such as TATA-binding protein and transcription factor IIB were carried out. A direct interaction between IE4 and TATA-binding protein or transcription factor IIB components of the basal complex of transcription was evidenced, as well as binding to the p50 and p65 NF-kappaB subunits. Mutagenesis analysis of IE4 indicated that the COOH-terminal cysteine-rich and arginine-rich regions (residues 82-182) were critical for transactivation, whereas the first 81 amino acids appeared dispensable. Moreover, the arginine-rich region is required for the in vitro binding activity, whereas the COOH-terminal end did not appear essential. [less ▲]

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See detailTraitement du cancer colorectal. Aspects pharmaco-économiques
Jerusalem, Guy ULg; Bours, Vincent ULg; Fillet, Georges ULg

in Revue Médicale de Liège (1998), 53(5), 276-8

Cancer patients care is mainly based on scientific studies, but sometimes approaches are empiric. Rapid growth of health care expenses force the physician to take pharmacoeconomic aspects into ... [more ▼]

Cancer patients care is mainly based on scientific studies, but sometimes approaches are empiric. Rapid growth of health care expenses force the physician to take pharmacoeconomic aspects into consideration. New clinical studies have to analyse clinical benefits but also cost-effectiveness. We will review the various aspects of colorectal cancer from primary prevention to post-treatment follow-up. Scientific data are integrated in a pharmacoeconomic analysis. [less ▲]

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See detailComment je traite ... Le cancer colorectal: I. Prévention et traitement adjuvant
Bours, Vincent ULg; Jerusalem, Guy ULg; Fillet, Georges ULg

in Revue Médicale de Liège (1998), 53(4), 167-70

Colorectal adenocarcinoma is a major cause of cancer-related morbidity and mortality in Belgium and in other western countries. Prevention implies a modification of alimentation and maybe a chronic uptake ... [more ▼]

Colorectal adenocarcinoma is a major cause of cancer-related morbidity and mortality in Belgium and in other western countries. Prevention implies a modification of alimentation and maybe a chronic uptake of acetylsalicylic acid. Treatment of colorectal cancers is based on surgery and the prognosis is determined by the locoregional or metastatic tumor spread. Complete resection of any Astler Coller stage C colorectal malignant tumor has to be followed by a 5-fluorouracil-based adjuvant chemotherapy. In these protocols, 5-fluorouracil is administered together with folinic acid or levamisole. The administration of an adjuvant chemotherapy could also be considered for stage BII diseases. As rectal cancers are characterized by high local relapse rates, their treatment should associate radiotherapy, given either post-surgery or preferentially pre-surgery, with resection and chemotherapy. Appropriate treatment of colorectal cancers thus requires a concerted multidisciplinary approach. [less ▲]

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See detailNuclear Factor - Kappab-Dependent Regulation of P53 Gene Expression Induced by Daunomycin Genotoxic Drug
Hellin, Anne-Cécile; Calmant, Philippe ULg; Bours, Vincent ULg et al

in Oncogene (1998), 16(9), 1187-95

Anthracycline drugs are widely used for the treatment of solid tumors and leukemia, but the molecular basis of their biological effect is still poorly understood. In the HCT116 colon carcinoma cell line ... [more ▼]

Anthracycline drugs are widely used for the treatment of solid tumors and leukemia, but the molecular basis of their biological effect is still poorly understood. In the HCT116 colon carcinoma cell line, which retains a wild-type inducible p53 gene, we show that the anthracycline daunomycin is a potent inducer of p53 and NF-kappaB transcription factors. Nuclear accumulation of p53 protein occurred because of increased protein stability and enhanced gene expression. In addition, daunomycin induced the p53 promoter through the binding of p50/p65 NF-kappaB heterodimers to the kappaB site in the p53 promoter. Under our conditions, the free radical scavengers NAC and PDTC were not able to block NF-kappaB activation or p53 induction, indicating that reactive oxygen intermediates were not involved in the cellular response to daunomycin stimulation. Overexpression of a stable unresponsive IkappaBalpha mutant in HCT116 cells resulted in a complete inhibition of the NF-kappaB activation but only a partial impairment of the p53 protein accumulation induced by daunomycin. We conclude that the p53-activating signal generated by daunomycin is partially regulated by NF-kappaB. [less ▲]

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See detailRegulation of major histocompatibility complex class I expression by NF-kB-related proteins in breast cancer cells
Dejardin, Emmanuel ULg; Deregowski, Valérie; GREIMERS, Roland ULg et al

in Oncogene (1998)

Downregulation of MHC Class I antigens has been observed in many cancers and usually results from a decreased gene transcription. A reporter CAT gene dependent on the MHC Class I kB site or on a longer ... [more ▼]

Downregulation of MHC Class I antigens has been observed in many cancers and usually results from a decreased gene transcription. A reporter CAT gene dependent on the MHC Class I kB site or on a longer promoter is transactivated by NF-kB complexes contain- ing p65 or RelB. p100 as well as IkB-a are potent inhibitors of this transcription and p100 sequesters RelB and p65 complexes in the cytoplasm of breast cancer cells. However, although p100 is highly expressed in a number of breast cancer cell lines, MHC Class I antigen expression was observed on all the cell lines we analysed and could be further induced by stimulation with the cytokines IFN-g or TNF-a. Stable transfection of a unresponsive mutated IkB-a Ser 32-36 expression vector showed that TNF-a induced MHC Cl I expression in an NF-kB-dependent way while IFN-g did it independently of any NF-kB activation. [less ▲]

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See detailHsv-1 Thymidine Kinase Gene Therapy for Peritoneal Carcinomatosis
Lechanteur, Chantal ULg; Princen, Frédéric; Lo Bue, S. et al

in Advances in Experimental Medicine and Biology (1998), 451

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See detailDistinct Signal Transduction Pathways Mediate Nuclear Factor-Kappab Induction by Il-1beta in Epithelial and Lymphoid Cells
Bonizzi, Giuseppina; Piette, Jacques ULg; Merville, Marie-Paule ULg et al

in Journal of Immunology (1997), 159(11), 5264-72

We previously demonstrated that IL-1beta-mediated induction of the nuclear factor-kappaB (NF-kappaB) transcription factor proceeds through the production of reactive oxygen intermediates in lymphoid cells ... [more ▼]

We previously demonstrated that IL-1beta-mediated induction of the nuclear factor-kappaB (NF-kappaB) transcription factor proceeds through the production of reactive oxygen intermediates in lymphoid cells, while it occurs independently of any oxidative stress in epithelial transformed cells. Indeed, inhibition of receptor internalization as well as NH4Cl and chloroquine blocked IL-1beta-mediated induction of NF-kappaB in OVCAR-3 and in other epithelial cell lines but not in lymphoid cells, indicating that distinct pathways are involved. Conversely, while we observed phospholipase A2 activity in both cell types following IL-1beta stimulation, specific inhibitors of this enzyme inhibited NF-kappaB induction only in lymphoid cells. Moreover, expression of the 5-lipoxygenase (5-LOX) enzyme was not detected in epithelial cells, and inhibition of this enzyme blocked NF-kappaB induction by IL-1beta only in lymphoid cells. This study thus indicates that the activation of NF-kappaB following IL-1beta treatment involves the activation of phospholipase A2 and 5-LOX and the production of reactive oxygen intermediates (ROIs) in lymphoid cells, while in epithelial cells, another pathway predominates and could involve the acid sphingomyelinase. Moreover, arachidonic acid could induce NF-kappaB in epithelial and lymphoid cells, but this activation involved the 5-LOX enzyme and the production of ROIs only in lymphoid cells. The inefficiency of the ROI pathway in epithelial cells is probably the consequence of both low ROI production due to undetectable expression of 5-LOX and rapid degradation of hydrogen peroxide due to high catalase activity. [less ▲]

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See detailMultiple Redox Regulation in Nf-Kappab Transcription Factor Activation
Piette, Jacques ULg; Piret, Bernard; Bonizzi, Giuseppina et al

in Biological Chemistry (1997), 378(11), 1237-45

The well-known Rel/NF-kappaB family of vertebrate transcription factors comprises a number of structurally related, interacting proteins that bind DNA as dimers and whose activity is regulated by ... [more ▼]

The well-known Rel/NF-kappaB family of vertebrate transcription factors comprises a number of structurally related, interacting proteins that bind DNA as dimers and whose activity is regulated by subcellular location. This family includes many members (p50, p52, RelA, RelB, c-Rel, ...), most of which can form DNA-binding homo- or hetero-dimers. All Rel proteins contain a highly conserved domain of approximately 300 amino-acids, called the Rel homology domain (RH), which contains sequences necessary for the formation of dimers, nuclear localization, DNA binding and IkappaB binding. Nuclear expression and consequent biological action of the eukaryotic NF-kappaB transcription factor complex are tightly regulated through its cytoplasmic retention by ankyrin-rich inhibitory proteins known as IkappaB. The IkappaB proteins include a group of related proteins that interact with Rel dimers and regulate their activities. The interaction of a given IkappaB protein with a Rel complex can affect the Rel complex in distinct ways. In the best characterized example, IkappaB-alpha interacts with a p50/RelA (NF-kappaB) heterodimer to retain the complex in the cytoplasm and inhibit its DNA-binding activity. The NF-kappaB/IkappaB-alpha complex is located in the cytoplasm of most resting cells, but can be rapidly induced to enter the cell nucleus. Upon receiving a variety of signals, many of which are probably mediated by the generation of reactive oxygen species (ROS), IkappaB-alpha undergoes phosphorylation at serine residues by a ubiquitin-dependent protein kinase, is then ubiquitinated at nearby lysine residues and finally degraded by the proteasome, probably while still complexed with NF-kappaB. Removal of IkappaB-alpha uncovers the nuclear localization signals on subunits of NF-kappaB, allowing the complex to enter the nucleus, bind to DNA and affect gene expression. Like proinflammatory cytokines (e.g. IL-1, TNF), various ROS (peroxides, singlet oxygen, ...) as well as UV (C to A) light are capable of mediating NF-kappaB nuclear translocation, while the sensor molecules which are sensitive to these agents and trigger IkappaB-alpha proteolysis are still unidentified. We also show that a ROS-independent mechanism is activated by IL-1beta in epithelial cells and seems to involve the acidic sphingomyelinase/ceramide transduction pathway. [less ▲]

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See detailHsv-1 Thymidine Kinase Gene Therapy for Colorectal Adenocarcinoma-Derived Peritoneal Carcinomatosis
Lechanteur, Chantal ULg; Princen, Frédéric; Lo Bue, S. et al

in Gene Therapy (1997), 4(11), 1189-94

Peritoneal carcinomatosis is a common clinical situation which, in most cases, cannot be eradicated by surgery or chemotherapy. The feasibility of an HSV-TK-based suicide gene therapy for peritoneal ... [more ▼]

Peritoneal carcinomatosis is a common clinical situation which, in most cases, cannot be eradicated by surgery or chemotherapy. The feasibility of an HSV-TK-based suicide gene therapy for peritoneal carcinomatosis induced by DHD/K12 colon carcinoma cells was investigated. DHD/K12 cells stably expressing the tk gene were killed in vitro in the presence of low concentrations of ganciclovir, they exhibited a 'bystander effect' when mixed with TK-negative cells. BD-IX rats injected intraperitoneally, either directly or after surgical peritoneal irritations, with DHD/K12 cells developed peritoneal carcinomatosis within 2 weeks. Ganciclovir treatment of animals injected with DHD/K12-TK cells allowed a significant reduction of the tumor volume as well as a prolonged survival. Of these animals 35-40% showed a long-term disease-free survival after ganciclovir therapy. Residual or relapsing tumors could be explained by a low expression of the transgene as demonstrated by RT-PCR. [less ▲]

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See detailInterleukin-1 Beta Induces Nuclear Factor Kappa B in Epithelial Cells Independently of the Production of Reactive Oxygen Intermediates
Bonizzi, Giuseppina; Dejardin, Emmanuel ULg; Piret, Bernard et al

in European Journal of Biochemistry (1996), 242(3), 544-9

A large body of work has been devoted to tumor necrosis factor alpha or interleukin-1 beta (IL-1 beta) signaling leading to the activation of the transcription factor nuclear factor-kappa B (NF-kappa B ... [more ▼]

A large body of work has been devoted to tumor necrosis factor alpha or interleukin-1 beta (IL-1 beta) signaling leading to the activation of the transcription factor nuclear factor-kappa B (NF-kappa B) in various cell types. Several studies have indicated that NF-kappa B activation depends strictly on the production of reactive oxygen intermediates. In this report, we first demonstrated that IL-1 beta is a potent activator of NF-kappa B in various epithelial transformed cell lines (OVCAR-3, SKOV-3, MCF7 A/Z). In these cells, IL-1 beta rapidly induces NF-kappa B through a complete degradation of I kappa B-alpha, while H2O2 activates NF-kappa B with slower kinetics through a partial degradation of I kappa B-alpha, p100 and p105. We showed that IL-1 beta-mediated induction of NF-kappa B in OVCAR-3 and in other epithelial cell lines does not proceed through the production of reactive oxygen intermediates, while the same cytokine activates NF-kappa B in lymphoid cells through the intracellular generation of H2O2. Our study demonstrated that several signaling pathways lead to the activation of NF-kappa B, following IL-1 beta treatment in different cell types. [less ▲]

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See detailRétinoïdes et leucémie aigue promyelocytaire. Une révolution thérapeutique
Hermanne, Jean-Philippe; Tassin, Françoise ULg; Bours, Vincent ULg et al

in Revue Médicale de Liège (1996), 51(3), 217-23

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See detailIntérêt de l'acide rétinoïque "tous trans" dans le traitement de la leucémie aiguë promyélocytaire
Hermanne, J.-P.; Tassin, F.; Bours, Vincent ULg et al

in Médecine et Hygiène (1996), 54

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See detailHighly-Expressed P100/P52 (Nfkb2) Sequesters Other Nf-Kappa B-Related Proteins in the Cytoplasm of Human Breast Cancer Cells
Dejardin, Emmanuel ULg; Bonizzi, Giuseppina; Bellahcene, Akeila ULg et al

in Oncogene (1995), 11(9), 1835-41

Several observations have suggested that NF-kappa B transcription factors could be involved in carcinogenesis. To investigate the possibility that members of the NF-kappa B family participate in the ... [more ▼]

Several observations have suggested that NF-kappa B transcription factors could be involved in carcinogenesis. To investigate the possibility that members of the NF-kappa B family participate in the molecular control of the transformed phenotype, we examined the expression of these proteins in human breast cancer cell lines as well as in primary tumors. Western Immunoblots demonstrated high expression of the p52 precursor p100 (NFKB2) in several breast cancer cell lines while human mammary epithelial cells express this protein only faintly. Eighteen primary breast tumors out of 24 displayed significant expression of the p100/p52 protein. In MDA-MB-435 cells, overexpressed p100 and p52 are predominantly cytoplasmic and coimmunoprecipitation experiments demonstrated that p100 sequesters the heterodimer p50/p65 in the cytoplasm. We demonstrate that most p65 protein is complexed with p100 in these cells while it is complexed predominantly with I kappa B-alpha in cell lines expressing less p100. Our data strengthen the hypothesis that NF-kappa B could be involved in carcinogenesis and suggest that the p100/p52 NF-kappa B subunit could play a role in the development of human breast cancers, possibly by sequestering other NF-kappa B-related proteins in the cytoplasm. [less ▲]

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See detailTranscription factor NF-kB is activated by photosensitization generating oxidative DNA damages
Legrand-Poels, Sylvie ULg; Bours, Vincent ULg; Piret, Bernard et al

in Journal of Biological Chemistry (1995), 270(12), 6925-6934

Reactive oxygen intermediates like hydrogen peroxide (H2O2) have been shown to serve as messengers in the induction of NF-kappa B and, then, in the activation and replication of human immunodeficiency ... [more ▼]

Reactive oxygen intermediates like hydrogen peroxide (H2O2) have been shown to serve as messengers in the induction of NF-kappa B and, then, in the activation and replication of human immunodeficiency virus (HIV)-1 in human cells. Because H2O2 can be converted into the highly reactive OH. at various locations inside the cells, we started to investigate the generation of Reactive oxygen intermediates by photosensitization. This technique is based on the use of a photosensitizer which is a molecule absorbing visible light and which can be located at various sites inside the cell depending on its physicochemical properties. In this work, we used proflavine (PF), a cationic molecule having a high affinity for DNA, capable of intercalating between DNA base pairs. Upon visible light irradiation, intercalated PF molecules oxidize guanine residues and generate DNA single-strand breaks. In lymphocytes or monocytes latently infected with HIV-1 (ACH-2 or U1, respectively), this photosensitizing treatment induced a cytotoxicity, an induction of NF-kappa B, and a reactivation of HIV-1 in cells surviving the treatment. NF-kappa B induction by PF-mediated photosensitization was not affected by the presence of N-acetyl-L-cysteine while strong inhibition was recorded when the induction was triggered by H2O2 or by phorbol 12-myristate 13-acetate. Another transcription factor like AP-1 is less activated by this photosensitizing treatment. In comparison with other inducing treatments, such as phorbol 12-myristate 13-acetate or tumor necrosis factor alpha, the activation of NF-kappa B is slow, being optimal 120 min after treatment. These kinetic data were obtained by following, on the same samples, both the appearance of NF-kappa B in the nucleus and the disappearance of I kappa B-alpha in cytoplasmic extracts. These data allow us to postulate that signaling events, initiated by DNA oxidative damages, are transmitted into the cytoplasm where the inactive NF-kappa B factor is resident and allow the translocation of p50/p65 subunits of NF-kappa B to the nucleus leading to HIV-1 gene expression. [less ▲]

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