Journal articles: 'Inducibility'

1

Dossou-Olory, Audace A. V., and Stephan Wagner. "Inducibility of topological trees." Quaestiones Mathematicae 42, no. 6 (August 8, 2018): 749–64. http://dx.doi.org/10.2989/16073606.2018.1497725.

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Choi, Ilkyoo, Bernard Lidický, and Florian Pfender. "Inducibility of directed paths." Discrete Mathematics 343, no. 10 (October 2020): 112015. http://dx.doi.org/10.1016/j.disc.2020.112015.

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Czabarka, Éva, Audace A. V. Dossou-Olory, László A. Székely, and Stephan Wagner. "Inducibility of d-ary trees." Discrete Mathematics 343, no. 2 (February 2020): 111671. http://dx.doi.org/10.1016/j.disc.2019.111671.

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Hefetz, Dan, and Mykhaylo Tyomkyn. "On the inducibility of cycles." Journal of Combinatorial Theory, Series B 133 (November 2018): 243–58. http://dx.doi.org/10.1016/j.jctb.2018.04.008.

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RAMIREZ, J., F. INNOCENTI, B. KOMOROSKI, S. MIRKOV, A. YODERGRABER, D. FACKENTHAL, S. DAS, E. SCHUETZ, S. STROM, and M. RATAIN. "Genetic determinants of UGT1A1 inducibility." Clinical Pharmacology & Therapeutics 77, no. 2 (February 2005): P25. http://dx.doi.org/10.1016/j.clpt.2004.11.096.

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Hefetz, Dan, and Mykhaylo Tyomkyn. "On the inducibility of cycles." Electronic Notes in Discrete Mathematics 61 (August 2017): 593–99. http://dx.doi.org/10.1016/j.endm.2017.07.012.

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Messier, H., J. Ratanavongsiri, T. Fuller, S. Mangal, P. Kilgannon, R. Fotedar, and A. Fotedar. "Mapping of an inducible element in the T cell receptor V beta 2 promoter." Journal of Immunology 149, no. 6 (September 15, 1992): 1980–86. http://dx.doi.org/10.4049/jimmunol.149.6.1980.

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Abstract The murine V beta 2 promoter was analyzed for an element regulating phorbol ester inducibility of the TCR beta chain gene. In transient expression analysis of 5' nested deleted fragments of the V beta 2 promoter, the TPA-inducible element mapped between -85 and -42. The -85 to -62 oligo conferred 12-0-tetradecanoylphorbol-13-acetate (TPA) inducibility to the heterologous TPA-uninducible thymidine kinase promoter. The -85 to -62 region contained an AP-1 site (-85 to -72) and inverted repeat motif (-72 to -62). The AP-1 site required the 3' flanking inverted repeat region for conferring optimal inducibility. In vitro transcribed and translated jun/fos heterodimers bind to the V beta 2 AP-1 motif with a 16-fold lower affinity as compared to the collagenase AP-1 motif. This explains the inability of the V beta 2 AP-1 motif to confer optimal TPA inducibility by itself. The affinity of jun/fos heterodimers for the V beta 2 AP-1 motif was not increased by the presence in cis of the inverted repeat motif. The 3' flanking inverted repeat binds the ets transactivator but not jun/fos heterodimers. The demonstrated cooperativity between the AP-1 and the 3' flanking sequence to confer TPA inducibility can thus be explained by the individual contributions of jun/fos and ets transactivators.

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Uliana Trentin, Henrique, Grigorii Batîru, Ursula Karoline Frei, Somak Dutta, and Thomas Lübberstedt. "Investigating the Effect of the Interaction of Maize Inducer and Donor Backgrounds on Haploid Induction Rates." Plants 11, no. 12 (June 7, 2022): 1527. http://dx.doi.org/10.3390/plants11121527.

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Doubled haploid technology is a feasible, fast, and cost-efficient way of producing completely homozygous lines in maize. Many factors contribute to the success of this system including the haploid induction rate (HIR) of inducer lines, the inducibility of donor background, and environmental conditions. Sixteen inducer lines were tested on eight different genetic backgrounds of five categories in different environments for the HIR to determine possible interaction specificity. The HIR was assessed using the R1-nj phenotype and corrected using the red root marker or using a gold-standard test that uses plant traits. RWS and Mo-17-derived inducers showed higher average induction rates and the commercial dent hybrid background showed higher inducibility. In contrast, sweet corn and flint backgrounds had a relatively lower inducibility, while non-stiff stalk and stiff stalk backgrounds showed intermediate inducibility. For the poor-performing donors (sweet corn and flint), there was no difference in the HIR among the inducers. Anthocyanin inhibitor genes in such donors were assumed to have increased the misclassification rate in the F1 fraction and, hence, result in a lower HIR.

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MATSUO, YOSHINORI, and TSUNEYUKI YAMAZAKI. "Genetic factors on the second and third chromosomes responsible for the variation of amylase activity and inducibility in Drosophila melanogaster." Genetical Research 70, no. 2 (October 1997): 97–103. http://dx.doi.org/10.1017/s0016672397002887.

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Using second- or third-chromosome substitution lines of Drosophila melanogaster, the genetic variation of inducibility and amylase specific activities in three media (starch, normal and glucose) were investigated. Genetic factors on both the second and third chromosomes were responsible for the variation in amylase specific activity and inducibility. In glucose medium, the genetic variance of amylase specific activity estimated for the second-chromosome substitution lines was larger than that for the third-chromosome substitution lines; however, for starch medium and inducibility, the variance was larger for the third-chromosome substitution lines. High correlations for the second-chromosome substitution lines and low correlations for the third-chromosome substitution lines were observed for amylase specific activities in different media. These results suggest that the genetic factor(s) responsible for inducibility or amylase activity variation in an induced medium such as starch should be on the third chromosome and those in the non-induced medium such as glucose should be on the second chromosome. The functional roles of the factors on the second and third chromosomes would be the repression and induction of amylase, respectively.

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Massa, P. T., R. Brinkmann, and V. ter Meulen. "Inducibility of Ia antigen on astrocytes by murine coronavirus JHM is rat strain dependent." Journal of Experimental Medicine 166, no. 1 (July 1, 1987): 259–64. http://dx.doi.org/10.1084/jem.166.1.259.

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Inducibility of Ia molecules on cultivated astrocytes by JHM virus correlates with demyelinating disease susceptibility of animals from which these astrocytes are derived. On the contrary, class I induction of both astrocytes and oligodendrocytes occurs as a consequence of normal cultivation procedures in both susceptible and resistant strains. Increased expression of class I antigens on rat astrocytes and oligodendrocytes is not related to JHM viral infection as it is in the mouse. These data indicate that strain differences in Ia inducibility, rather than inducibility of class I antigens, by JHM virus may explain higher levels of T cell-mediated damage to myelin during infection in susceptible rat strains compared with resistant strains.

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Lader, Joshua M., Carolina Vasquez, Li Bao, Karen Maass, Jiaxiang Qu, Eirini Kefalogianni, Glenn I. Fishman, William A. Coetzee, and Gregory E. Morley. "Remodeling of atrial ATP-sensitive K+ channels in a model of salt-induced elevated blood pressure." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 2011): H964—H974. http://dx.doi.org/10.1152/ajpheart.00410.2011.

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Hypertension is associated with the development of atrial fibrillation; however, the electrophysiological consequences of this condition remain poorly understood. ATP-sensitive K+ (KATP) channels, which contribute to ventricular arrhythmias, are also expressed in the atria. We hypothesized that salt-induced elevated blood pressure (BP) leads to atrial KATP channel activation and increased arrhythmia inducibility. Elevated BP was induced in mice with a high-salt diet (HS) for 4 wk. High-resolution optical mapping was used to measure atrial arrhythmia inducibility, effective refractory period (ERP), and action potential duration at 90% repolarization (APD90). Excised patch clamping was performed to quantify KATP channel properties and density. KATP channel protein expression was also evaluated. Atrial arrhythmia inducibility was 22% higher in HS hearts compared with control hearts. ERP and APD90 were significantly shorter in the right atrial appendage and left atrial appendage of HS hearts compared with control hearts. Perfusion with 1 μM glibenclamide or 300 μM tolbutamide significantly decreased arrhythmia inducibility and prolonged APD90 in HS hearts compared with untreated HS hearts. KATP channel density was 156% higher in myocytes isolated from HS animals compared with control animals. Sulfonylurea receptor 1 protein expression was increased in the left atrial appendage and right atrial appendage of HS animals (415% and 372% of NS animals, respectively). In conclusion, KATP channel activation provides a mechanistic link between salt-induced elevated BP and increased atrial arrhythmia inducibility. The findings of this study have important implications for the treatment and prevention of atrial arrhythmias in the setting of hypertensive heart disease and may lead to new therapeutic approaches.

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Eades, A. M., M. Litfin, and H. J. Rahmsdorf. "The IFN-gamma response of the murine invariant chain gene is mediated by a complex enhancer that includes several MHC class II consensus elements." Journal of Immunology 144, no. 11 (June 1, 1990): 4399–409. http://dx.doi.org/10.4049/jimmunol.144.11.4399.

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Abstract IFN-gamma induces the expression of the MHC class II-associated invariant chain (IN) protein in a variety of cells of nonlymphoid origin. Here we analyze the transcription from the murine invariant chain gene and delimit the cis-acting sequences which confer IFN-gamma responsiveness in human fibroblasts. The major start of transcription of the gene is located 29 bp 3' of a TATA box and 85 bp 5' of the single ATG codon which opens the reading frame. To identify the regulatory elements of the murine IN promoter which respond to IFN-gamma, the 5' flanking region of the gene including its capsite and 85 bp of coding region have been cloned in front of the bacterial chloramphenicol acetyl transferase (CAT) gene. Examination of this construct and various 5' and 3' deletion mutants for IFN-gamma inducibility in transient transfection assays revealed that DNA sequences between -261 and -189 were essential and sufficient for the induction. Removal of sequences between -215 and -189 reduced inducibility of the IN-promoter and abolished the capacity of the element to transmit inducibility to a heterologous promoter. Single or multiple base changes in other parts of the element also abolished inducibility. Cotransfection of a 350 molar excess of the IFN-gamma response element with an inducible IN-CAT chimeric construct blocked inducibility, suggesting positive regulation. A protein binding to the central part of the IFN-gamma response element was detectable in gel retardation experiments; it was active only in extracts from IFN-gamma-treated cells.

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13

Lu, Y., J. M. Boss, S. X. Hu, H. J. Xu, and G. Blanck. "Apoptosis-independent retinoblastoma protein rescue of HLA class II messenger RNA IFN-gamma inducibility in non-small cell lung carcinoma cells. Lack of surface class II expression associated with a specific defect in HLA-DRA induction." Journal of Immunology 156, no. 7 (April 1, 1996): 2495–502. http://dx.doi.org/10.4049/jimmunol.156.7.2495.

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Abstract Work from our laboratory indicates that HLA class II induction by IFN- gamma in the retinoblastoma (RB) protein-defective breast carcinoma line MDA-468-S4 (S4) requires reconstitution of functional RB. To determine whether RB is required for HLA class 11 expression in multiple tumor types, the RB-defective non-small cell lung carcinoma line H2009 and its RB-reconstituted subclones were examined for class II inducibility. Surface HLA-DR (DR) was not inducible by IFN-gamma in H2009. However, unlike the RB-reconstituted subclones of S4, DR surface expression was not detected in the H2009 RB-positive subclones. IFN-gamma induction of CIITA, a major regulator of class II transcription, suggested that H2009 retained at least part of the IFN-gamma signaling pathway leading to class II expression. Examination of class II mRNA indicated that IFN-gamma induction of RB was rescued in the RB-positive subclones of H2009, confirming the requirement for RB for HLA class II inducibility and revealing that RB is required for inducibility in developmentally distinct tumor types. However, DRA inducibility was not rescued in the H2009 RB-positive subclones, which explained the lack of surface DR induction in the RB-positive H2009 subclones. DPA and DPB were also only weakly inducible in the RB-reconstituted H2009 subclones, compared with the previously described, S4 RB-positive subclones. Finally, data reported here indicates that RB's ability to inhibit IFN-gamma-induced apoptosis is not a viable explanation for why RB expression rescues DRB inducibility in H2009.

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Chumchalova, Jitka, Dana Klimesova, Viera Kuhrova, Hana Francova, Yvona Brychtova, Michael Doubek, Dana Dvorakova, and Jiri Mayer. "Constitutive Activation of STAT1 and STAT3 Proteins on Serine and Tyrosine Residues Were Found in Majority of CLL Patients." Blood 108, no. 11 (November 16, 2006): 4931. http://dx.doi.org/10.1182/blood.v108.11.4931.4931.

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Abstract Background: Chronic lymphocytic leukemia (CLL) is the most common form of adult leukemia in the world. CLL is currently an incurable disease, characterized by the gradual accumulation of mature B-lymphocytes arrested in the G0 phase of the cell cycle. STAT (signal transducers and activators of transcription) proteins are involved in normal cellular events, such as differentiation, proliferation, cell survival, apoptosis and hematopoiesis. STAT proteins are constitutively activated in hematopoetic cells transformed by oncogenic tyrosine kinases and also in a variety of leukemias and lymphomas. The tyrosine phosphorylation of the STATs allows formation of dimmers, translocation to the nucleus and bindind of specific DNA sequences in the promoters of target genes, leading to activation of transcription. Serine phosphorylation is not sufficient to activate the STAT, providing a degree of modulation of the gene activation induced by the tyrosine phosphorylation. Serine phosphorylation of STAT1 and STAT3 has been described in untreated B-CLL cells, but no constitutive tyrosine phosphorylation has been detected in B-CLL cells. Aims: Aim of our study was to examine defects in STAT1 and STAT3 pathways in our CLL patients. Methods: We analyzed defects in STAT1 and STAT3 pathways after stimulation of cells with 10 ng/ml IFNγ and 5000 IU/ml IFNα in 42 primary cultures derived from CLL patients. STAT1 and STAT3 inducibilities of their activated phospho-isoforms were detected by Western-blotting analysis using specific polyclonal and monoclonal antibodies. Results: Constitutive phosphorylation of STAT1 and STAT3 proteins was detected in majority of patients (STAT1 PS727 95.2%, STAT3 PS727 90,6 %, STAT1 PY701 85,7% and STAT3 PY705 79,4%). The IFNα was shown to be a more effective inductor in comparison with IFNγ. The inducibility after IFNα with constitutive activation of both STAT proteins on serine and tyrosine was the most frequently detected. Inducibility after IFNα with constitutive activation at STAT1 PY701 was found in 61,9 % of samples, with 21,4% having the inducibility after both IFNs. Inducibility after IFNα at STAT3 PY705 was detected in 88,2% of cases, with 70,6% having a constitutive activation and 20,5% having not. Inducibility after IFNα with constitutive activation at both serine residues is the most commonly observed pattern (STAT1 PS727 40.5%, STAT3 PS727 70,6 %). A high proportion of patients had constitutive activation with no inducibility at serine (STAT1 PS727 47,6%, STAT3 PS727 28,1 %) compared to that at tyrozine (STAT1 PY701 19%, STAT3 PY705 2,9). The inducibility after IFNγ did not exceed 10 % in all cases. Conclusions: Our results show constitutive phosphorylation of STAT1 and STAT3 proteins on both serine and tyrosine residues in most of our CLL patients. More effective inductor is the IFNα. Approximately a half of patients have defect of inducibility in serine phosphorylation of STAT1 protein.

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Xiaokereti, Jiasuoer, Yan-Kai Guo, Zhen-Yu Dong, Mei Ma, Yan-Mei Lu, Yao-Dong Li, Xian-Hui Zhou, Ling Zhang, and Bao-Peng Tang. "Enhanced atrial internal-external neural remodeling facilitates atrial fibrillation in the chronic obstructive sleep apnea model." PLOS ONE 16, no. 2 (February 19, 2021): e0247308. http://dx.doi.org/10.1371/journal.pone.0247308.

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Objective Autonomic imbalance plays a crucial role in obstructive sleep apnea (OSA) associated atrial fibrillation (AF). Here, we investigated the potential neural mechanism of AF induced by OSA. Methods Ten dogs were divided into control group (n = 5) and OSA group (n = 5). The chronic OSA model was established by repeat apnea-ventilation cycles for 4 hours a day for 12 weeks. During the process of model establishment, arterial blood gases, atrial effective refractory period (AERP), AF inducibility, normalized low-frequency power (LFnu), normalized high-frequency power (HFnu), and LFnu/ HFnu were evaluated at baseline, 4th week, 8th week, and 12th week. Nerve activities of left stellate ganglion (LSG) and left vagal nerve(LVN) were recorded. Tyrosine hydroxylase(TH), choline acetyltransferase(CHAT), PGP9.5, nerve growth factor(NGF), and c-Fos were detected in the left atrium, LSG, and LVN by immunohistochemistry and western blot. Moreover, high-frequency stimulations of LSG and LVN were conducted to observe the AF inducibility. Results Compared with the control group, the OSA group showed significantly enhanced neural activity of the LSG, increased AF inducibility, and shortened AERP. LFnu and LFnu/HFnu were markedly increased in the OSA group, while no significant difference in HFnu was observed. TH-positive and PGP9.5-positive nerve densities were significantly increased in the LSG and left atrium. Additionally, the protein levels of NGF, c-Fos, and PGP9.5 were upregulated both in the LSG and left atrium. AF inducibility was markedly increased under LSG stimulation without a stimulus threshold change in the OSA group. Conclusions OSA significantly enhanced LSG and left atrial neural remodeling, and hyperactivity of LSG may accelerate left atrial neural remodeling to increase AF inducibility.

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Lee, Jae S., Lisa Greco, Allan Migirov, Ying Li, A. Martin Gerdes, and Youhua Zhang. "Chronic Dantrolene Treatment Does Not Affect Hypertension, but Attenuates Sympathetic Stimulation Enhanced Atrial Fibrillation Inducibility in SHR." American Journal of Hypertension 33, no. 5 (February 15, 2020): 407–13. http://dx.doi.org/10.1093/ajh/hpaa021.

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Abstract Background Ryanodine receptor (RyR) dysfunction in skeletal muscle (RyR1) leads to malignant hyperthermia, and in cardiac muscle (RyR2) triggers cardiac arrhythmias. We hypothesized that RyR dysfunction in vascular smooth muscle could increase vascular resistance and hypertension, and may contribute to increased atrial fibrillation (AF) in hypertension. Thus, stabilizing RyR function with chronic dantrolene treatment may attenuate hypertension and AF inducibility in spontaneously hypertensive rats (SHR). Methods Male SHR (16 weeks old) were randomized into vehicle- (n = 10) and dantrolene-treated (10 mg/kg/day, n = 10) groups for 4 weeks. Wistar Kyoto (WKY, n = 11) rats served as controls. Blood pressures (BP) were monitored before and during the 4-week treatment. After 4-week treatment, direct BP, echocardiography, and hemodynamics were recorded. AF inducibility tests were performed in vivo at baseline and repeated under sympathetic stimulation (SS). Results Compared with WKY, SHR had significantly higher BP throughout the experimental period. Dantrolene treatment had no effect on BP levels in SHR (final systolic BP 212 ± 9 mm Hg in vehicle group vs. 208 ± 16 mm Hg in dantrolene group, P > 0.05). AF inducibility was very low and not significantly different between 5-month-old WKY and SHR at baseline. However, under SS, AF inducibility and duration were significantly increased in SHR (20% in WKY vs. 60% in SHR-vehicle, P<0.05). Dantrolene treatment significantly attenuated AF inducibility under SS in SHR (60% in vehicle vs. 20% in dantrolene, P < 0.05). Conclusions Stabilizing RyR with chronic dantrolene treatment does not affect hypertension development in SHR. SHR has increased vulnerability to AF induction under SS, which can be attenuated with dantrolene treatment.

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Kaempfer, R., L. Gerez, H. Farbstein, L. Madar, O. Hirschman, R. Nussinovich, and A. Shapiro. "Prediction of response to treatment in superficial bladder carcinoma through pattern of interleukin-2 gene expression." Journal of Clinical Oncology 14, no. 6 (June 1996): 1778–86. http://dx.doi.org/10.1200/jco.1996.14.6.1778.

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PURPOSE Superficial bladder carcinoma, treated by resection and intravesical administration of bacillus Calmette-Guérin (BCG), yields a remission rate that approaches 70%. We examined whether expression of interleukin-2 (IL-2) or interferon-gamma (IFN-gamma) genes can serve to predict response. PATIENTS AND METHODS During BCG treatment, we analyzed induction of IL-2 and IFN-gamma mRNA in peripheral-blood mononuclear cells (PBMC) from 73 patients: 51 with papillary tumors and 22 with carcinoma-in-situ (CIS). Results were correlated with remission, relapse, or tumor persistence over a 4-year follow-up period. RESULTS Independent of tumor type, induction of IL-2 mRNA was observed for patients who responded with remission, but not for those who relapsed (P = .0001). Multivariate logistic analysis showed that inducibility of IL-2 mRNA is the discriminating parameter, which yields a predictive value of 97% for remission. Of 23 patients with relapse/persistence, 22 lacked inducibility of IL-2 mRNA (sensitivity, 95.6%), while 35 of 50 patients in remission exhibited inducibility (specificity, 70%). For patients with carcinoma-in-situ, in which remission or failure depends solely on response to BCG, sensitivity and specificity were 88% and 86%, respectively; for patients with papillary tumors, they were 100% and 64%. IFN-gamma mRNA, by contrast, was clearly inducible in PBMC from all patients (P = .51). The disease-free interval increased progressively with inducibility of IL-2 mRNA; this trend was highly significant (P = .0001). CONCLUSION IL-2 gene expression is essential for mounting an antitumor response in superficial bladder carcinoma. Inducibility of IL-2 mRNA is an independent prognostic parameter and useful predictive indicator of remission versus relapse.

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Satya Lakshmi, O., and N. M. Rao. "Evolving Lac repressor for enhanced inducibility." Protein Engineering, Design and Selection 22, no. 2 (November 21, 2008): 53–58. http://dx.doi.org/10.1093/protein/gzn069.

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Wilmes, Anja, Martin O. Leonard, and Paul Jennings. "Nrf2 inducibility of aldo-keto reductases." Toxicology Letters 221, no. 1 (July 2013): 39. http://dx.doi.org/10.1016/j.toxlet.2013.05.012.

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BREMBILLAPERROT, B. "132 Age and atrial fibrillation inducibility." European Heart Journal 24, no. 5 (March 2003): 9. http://dx.doi.org/10.1016/s0195-668x(03)93678-5.

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Ortiz, Mercedes, Jesús Almendral, Ramón López-Palop, Julian Villacastı́n, and Angel Arenal. "Determinants of inducibility of ventricular tachycardia." American Journal of Cardiology 87, no. 11 (June 2001): 1255–59. http://dx.doi.org/10.1016/s0002-9149(01)01545-4.

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Müssigbrodt, Andreas, Arash Arya, Livio Bertagnolli, Borislav Dinov, and Gerhard Hindricks. "To the Editor— Thoughts on inducibility." Heart Rhythm 16, no. 4 (April 2019): e37. http://dx.doi.org/10.1016/j.hrthm.2019.01.001.

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Hatami, Hamed, James Hirst, and Serguei Norine. "The inducibility of blow-up graphs." Journal of Combinatorial Theory, Series B 109 (November 2014): 196–212. http://dx.doi.org/10.1016/j.jctb.2014.06.005.

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Brown, Jason I., and Alexander Sidorenko. "The inducibility of complete bipartite graphs." Journal of Graph Theory 18, no. 6 (October 1994): 629–45. http://dx.doi.org/10.1002/jgt.3190180610.

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Gui, Le, Zhiwei Bao, Yinyu Jia, Xiaotong Qin, Zixi (Jack) Cheng, Jianhua Zhu, and Qing-Hui Chen. "Ventricular tachyarrhythmias in rats with acute myocardial infarction involves activation of small-conductance Ca2+-activated K+ channels." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 1 (January 1, 2013): H118—H130. http://dx.doi.org/10.1152/ajpheart.00820.2011.

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In vitro experiments have shown that the upregulation of small-conductance Ca2+-activated K+ (SK) channels in ventricular epicardial myocytes is responsible for spontaneous ventricular fibrillation (VF) in failing ventricles. However, the role of SK channels in regulating VF has not yet been described in in vivo acute myocardial infarction (AMI) animals. The present study determined the role of SK channels in regulating spontaneous sustained ventricular tachycardia (SVT) and VF, the inducibility of ventricular tachyarrhythmias, and the effect of inhibition of SK channels on spontaneous SVT/VF and electrical ventricular instability in AMI rats. AMI was induced by ligation of the left anterior descending coronary artery in anesthetized rats. Spontaneous SVT/VF was analyzed, and programmed electrical stimulation was performed to evaluate the inducibility of ventricular tachyarrhythmias, ventricular effective refractory period (VERP), and VF threshold (VFT). In AMI, the duration and episodes of spontaneous SVT/VF were increased, and the inducibility of ventricular tachyarrhythmias was elevated. Pretreatment in the AMI group with the SK channel blocker apamin or UCL-1684 significantly reduced SVT/VF and inducibility of ventricular tachyarrhythmias ( P < 0.05). Various doses of apamin (7.5, 22.5, 37.5, and 75.0 μg/kg iv) inhibited SVT/VF and the inducibility of ventricular tachyarrhythmias in a dose-dependent manner. Notably, no effects were observed in sham-operated controls. Additionally, VERP was shortened in AMI animals. Pretreatment in AMI animals with the SK channel blocker significantly prolonged VERP ( P < 0.05). No effects were observed in sham-operated controls. Furthermore, VFT was reduced in AMI animals, and block of SK channels increased VFT in AMI animals, but, again, this was without effect in sham-operated controls. Finally, the monophasic action potential duration at 90% repolarization (MAPD90) was examined in the myocardial infarcted (MI) and nonmyocardial infarcted areas (NMI) of the left ventricular epicardium. Electrophysiology recordings showed that MAPD90 in the MI area was shortened in AMI animals, and pretreatment with SK channel blocker apamin or UCL-1684 significantly prolonged MAPD90 ( P < 0.05) in the MI area but was without effect in the NMI area or in sham-operated controls. We conclude that the activation of SK channels may underlie the mechanisms of spontaneous SVT/VF and suseptibility to ventricular tachyarrhythmias in AMI. Inhibition of SK channels normalized the shortening of MAPD90 in the MI area, which may contribute to the inhibitory effect on spontaneous SVT/VF and inducibility of ventricular tachyarrhythmias in AMI.

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Rheaume, C., K. W. Barbour, J. Tseng-Crank, and F. G. Berger. "Molecular genetics of androgen-inducible RP2 gene transcription in the mouse kidney." Molecular and Cellular Biology 9, no. 2 (February 1989): 477–83. http://dx.doi.org/10.1128/mcb.9.2.477-483.1989.

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Androgen control of the RP2 gene in the mouse kidney has been modified during evolution. In inbred mice (Mus domesticus), the concentrations of mRNAs encoded by RP2 undergo a 10- to 12-fold induction in response to testosterone; in other Mus species (e.g., Mus hortulanus and Mus caroli), induction ranges from none to about two- to fourfold. In this communication, we show that androgens induced RP2 transcription in M. domesticus, although this induction may not have fully accounted for the increase in mRNA levels. Reduced mRNA inducibility in M. hortulanus and in several other species was associated with an absence of transcriptional induction. Analysis of an interspecies backcross population indicated that the difference in RP2 inducibility between M. domesticus and M. hortulanus was due to a single Mendelian locus tightly linked (0 of 47 recombinants) to RP2. The RP2 gene was found to contain at least two promoters, only one of which was highly sensitive to testosterone. These results indicate that induction of the RP2 mRNAs, as well as interspecies variations in RP2 inducibility, are primarily a consequence of effects on this promoter.

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Rheaume, C., K. W. Barbour, J. Tseng-Crank, and F. G. Berger. "Molecular genetics of androgen-inducible RP2 gene transcription in the mouse kidney." Molecular and Cellular Biology 9, no. 2 (February 1989): 477–83. http://dx.doi.org/10.1128/mcb.9.2.477.

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Androgen control of the RP2 gene in the mouse kidney has been modified during evolution. In inbred mice (Mus domesticus), the concentrations of mRNAs encoded by RP2 undergo a 10- to 12-fold induction in response to testosterone; in other Mus species (e.g., Mus hortulanus and Mus caroli), induction ranges from none to about two- to fourfold. In this communication, we show that androgens induced RP2 transcription in M. domesticus, although this induction may not have fully accounted for the increase in mRNA levels. Reduced mRNA inducibility in M. hortulanus and in several other species was associated with an absence of transcriptional induction. Analysis of an interspecies backcross population indicated that the difference in RP2 inducibility between M. domesticus and M. hortulanus was due to a single Mendelian locus tightly linked (0 of 47 recombinants) to RP2. The RP2 gene was found to contain at least two promoters, only one of which was highly sensitive to testosterone. These results indicate that induction of the RP2 mRNAs, as well as interspecies variations in RP2 inducibility, are primarily a consequence of effects on this promoter.

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Ho, Li-Chun, Ting-Yun Wu, Tsun-Mei Lin, Hung-Hsiang Liou, and Shih-Yuan Hung. "Indoxyl Sulfate Mediates the Low Inducibility of the NLRP3 Inflammasome in Hemodialysis Patients." Toxins 13, no. 1 (January 7, 2021): 38. http://dx.doi.org/10.3390/toxins13010038.

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The NLRP3 inflammasome is responsible for the maturation of caspase-1 and interleukin-1β (IL-1β). Despite the study about basal activity of the NLRP3 inflammasome in hemodialysis (HD) patients, little is known about its inducibility in the milieu of uremia. Peripheral blood mononuclear cells (PBMCs) isolated from 11 HD patients and 14 volunteers without a history of chronic kidney disease, as well as macrophages with or without the uremic toxin indoxyl sulfate (IS) pretreatment, underwent canonical NLRP3 inflammasome induction. Despite the high plasma levels of IL-1β in HD patients, caspase-1 and IL-1β in the PBMCs of HD patients remained predominantly immature and were not secreted in response to the canonical stimulus. In addition, while IS alone facilitated the inflammasome-independent secretion of IL-1β from macrophages, IS exposure before induction reduced the inducibility of the NLRP3 inflammasome, characterized by insufficient maturation of caspase-1. The low expression of inflammasome components, which was observed in both IS-pretreated cells and the PBMCs of HD patients, was probably responsible for the low inducibility.

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29

Khodadoust, Mehran M., Khuda Dad Khan, and Alfred L. M. Bothwell. "Complex Regulation of Ly-6E Gene Transcription in T Cells by IFNs." Journal of Immunology 163, no. 2 (July 15, 1999): 811–19. http://dx.doi.org/10.4049/jimmunol.163.2.811.

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Abstract The complexity of IFN-mediated regulation of the murine Ly-6E gene in T cell lines is highlighted by the following observations: 1) multiple regulatory regions are present within different parts of the Ly-6E promoter and are necessary for IFN inducibility of the Ly-6E gene, 2) multiple transcription factors including Oct-1 and Oct-2 and the high mobility group (HMG) protein HMGI(Y) bind to regulatory elements present within the G region required for both IFN-αβ and IFN-γ responses, 3) mutational analysis of the G region reveals that a complex interaction exists between the factors binding to this region as shown by their mutual interdependence for detection in DMSA, and 4) inhibition of expression of HMG proteins by antisense HMGI-C RNA in EL4 cells causes the loss of IFN-αβ and IFN-γ inducibility of the endogenous Ly-6 gene. These findings taken together suggest that, in response to IFN treatment, an HMG protein-dependent complex involving multiple regulatory factors is assembled and is required for IFN inducibility of the Ly-6E gene.

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30

Maguire, Colin T., Hiroko Wakimoto, Vickas V. Patel, Peter E. Hammer, Kimberlee Gauvreau, and Charles I. Berul. "Implications of ventricular arrhythmia vulnerability during murine electrophysiology studies." Physiological Genomics 15, no. 1 (September 29, 2003): 84–91. http://dx.doi.org/10.1152/physiolgenomics.00034.2003.

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Programmed ventricular stimulation is being performed for the provocation of ventricular arrhythmias in genetically engineered mice. Despite the high level of interest in this area of translational research, little attention has been given to differentiating between selectivity and specificity of induced ventricular tachycardia (VT) in phenotypically normal mice. We aimed to assess factors that may enhance inducibility of VT in wild-type (WT) mice. In vivo intracardiac electrophysiological studies (EPS) were performed in 230 WT mice of 4 strains. An octapolar electrode catheter was inserted into a jugular vein and advanced to the right atrium and ventricle. Baseline ventricular conduction, refractoriness, and arrhythmia inducibility were assessed using programmed electrical stimulation (PES) and burst pacing. We found that nonsustained VT (≥4 beats) was inducible in 68/230 (30%) mice. Duration of VT was 1.6 ± 2.4 s, and the longest episode lasted 24 s. VT inducibility differed by strain and age. Ventricular effective refractory period (VERP) was shorter in mice with inducible VT (44 ± 12 ms) compared with noninducible mice (61 ± 16 ms, P < 0.001). VERP increased with age ( P < 0.001), albeit with strain-related variability. We conclude that nonsustained VT in WT mice is reproducibly inducible and common. Genetic background variability may predispose certain strains to a higher incidence of arrhythmia induction. EPS methods impact prevalence and specificity of inducible VT. Increased VT inducibility was seen with shorter coupling intervals and application of tightly coupled extrastimuli techniques. These factors should be carefully considered when analyzing PES and burst pacing data in murine models to minimize false positives and optimize accuracy.

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31

Mahida, Saagar, and William G. Stevenson. "Reply to the Editor— Thoughts on inducibility." Heart Rhythm 16, no. 4 (April 2019): e37-e38. http://dx.doi.org/10.1016/j.hrthm.2019.01.003.

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32

Chung, King-Thom. "Carcinogenicity allergenicity and lupus-inducibility of arylamines." Frontiers in Bioscience 8, no. 1 (2016): 29–39. http://dx.doi.org/10.2741/748.

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Chung, King-Thom. "Carcinogenicity allergenicity and lupus-inducibility of arylamines." Frontiers in Bioscience 8, no. 1 (2016): 29–39. http://dx.doi.org/10.2741/e748.

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34

BREMBILLA‐PERROT, BÉATRICE, GUILLAUME BURGER, DANIEL BEURRIER, PIERRE HOURIEZ, MARC NIPPERT, HIELKHO MILJOEN, MARIUS ANDRONACHE, et al. "Influence of Age on Atrial Fibrillation Inducibility." Pacing and Clinical Electrophysiology 27, no. 3 (March 2004): 287–92. http://dx.doi.org/10.1111/j.1540-8159.2004.00429.x.

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35

Ghersi-Egea, J. F., B. Walther, R. Perrin, A. Minn, A. Minn, and G. Siest. "Inducibility of rat brain drug-metabolizing enzymes." European Journal of Drug Metabolism and Pharmacokinetics 12, no. 4 (October 1987): 263–65. http://dx.doi.org/10.1007/bf03189910.

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36

Král', Daniel, Sergey Norin, and Jan Volec. "A bound on the inducibility of cycles." Journal of Combinatorial Theory, Series A 161 (January 2019): 359–63. http://dx.doi.org/10.1016/j.jcta.2018.08.003.

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37

Gregus, Z., C. Madhu, and C. D. Klaassen. "Inducibility of glutathione S-transferases in hamsters." Cancer Letters 44, no. 2 (February 1989): 89–94. http://dx.doi.org/10.1016/0304-3835(89)90002-5.

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38

Hirst, James. "The Inducibility of Graphs on Four Vertices." Journal of Graph Theory 75, no. 3 (March 6, 2013): 231–43. http://dx.doi.org/10.1002/jgt.21733.

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39

DARVAS, Z., S. NAGAO, Y. NOZAWA, and G. CSABA. "Selective inducibility of microsomal cytochrome b in." Cell Biology International Reports 11, no. 8 (August 1987): 627. http://dx.doi.org/10.1016/0309-1651(87)90145-7.

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40

Yu, C. L., E. V. Prochownik, M. J. Imperiale, and R. Jove. "Attenuation of serum inducibility of immediate early genes by oncoproteins in tyrosine kinase signaling pathways." Molecular and Cellular Biology 13, no. 4 (April 1993): 2011–19. http://dx.doi.org/10.1128/mcb.13.4.2011-2019.1993.

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Immediate early genes involved in controlling cell proliferation are rapidly and transiently induced following stimulation of susceptible cells with serum. To study how oncoproteins regulate immediate early genes, we examined serum inducibility of these genes in cells transformed by various oncoproteins. We found that induction of the immediate early gene, c-fos, by serum stimulation was markedly attenuated in four independent cell lines stably transformed by the v-Src tyrosine kinase. Cells chronically transformed by other oncoproteins implicated in tyrosine kinase signaling pathways, including v-Sis, v-Ras, and v-Raf, showed the same pattern of attenuation. In contrast, serum inducibility of c-fos was not attenuated in cells transformed by simian virus 40, which is thought to transform cells through a different pathway. Cell cycle analyses showed that proliferation of these transformed cell lines could be arrested effectively in 0.1% serum, demonstrating that the attenuation was not simply due to continuous cycling of transformed cells after serum deprivation. Moreover, serum inducibility of other immediate early genes, including c-jun, junB, egr-1, and NGFI-B, also was strikingly attenuated by these same oncoproteins. Nuclear run-on transcription assays established that this attenuation of serum inducibility occurred at the transcriptional level. Finally, flow cytometric analysis demonstrated that serum-starved v-Src-transformed cells were viable and able to progress into S phase of the cell cycle after serum stimulation, even though the induction of immediate early genes was greatly attenuated in these cells. Our results suggest that activation of immediate early genes is repressed by chronic stimulation of tyrosine kinase signaling pathways in transformed cells.

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41

Yu, C. L., E. V. Prochownik, M. J. Imperiale, and R. Jove. "Attenuation of serum inducibility of immediate early genes by oncoproteins in tyrosine kinase signaling pathways." Molecular and Cellular Biology 13, no. 4 (April 1993): 2011–19. http://dx.doi.org/10.1128/mcb.13.4.2011.

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Immediate early genes involved in controlling cell proliferation are rapidly and transiently induced following stimulation of susceptible cells with serum. To study how oncoproteins regulate immediate early genes, we examined serum inducibility of these genes in cells transformed by various oncoproteins. We found that induction of the immediate early gene, c-fos, by serum stimulation was markedly attenuated in four independent cell lines stably transformed by the v-Src tyrosine kinase. Cells chronically transformed by other oncoproteins implicated in tyrosine kinase signaling pathways, including v-Sis, v-Ras, and v-Raf, showed the same pattern of attenuation. In contrast, serum inducibility of c-fos was not attenuated in cells transformed by simian virus 40, which is thought to transform cells through a different pathway. Cell cycle analyses showed that proliferation of these transformed cell lines could be arrested effectively in 0.1% serum, demonstrating that the attenuation was not simply due to continuous cycling of transformed cells after serum deprivation. Moreover, serum inducibility of other immediate early genes, including c-jun, junB, egr-1, and NGFI-B, also was strikingly attenuated by these same oncoproteins. Nuclear run-on transcription assays established that this attenuation of serum inducibility occurred at the transcriptional level. Finally, flow cytometric analysis demonstrated that serum-starved v-Src-transformed cells were viable and able to progress into S phase of the cell cycle after serum stimulation, even though the induction of immediate early genes was greatly attenuated in these cells. Our results suggest that activation of immediate early genes is repressed by chronic stimulation of tyrosine kinase signaling pathways in transformed cells.

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42

Sims, S. H., Y. Cha, M. F. Romine, P. Q. Gao, K. Gottlieb, and A. B. Deisseroth. "A novel interferon-inducible domain: structural and functional analysis of the human interferon regulatory factor 1 gene promoter." Molecular and Cellular Biology 13, no. 1 (January 1993): 690–702. http://dx.doi.org/10.1128/mcb.13.1.690-702.1993.

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We have cloned and functionally characterized the human interferon regulatory factor 1 (IRF-1) gene promoter. The promoter contains a CpG island, with several GC boxes, a CAAT box, but no TATA box. IRF-1 mRNA is strongly induced by gamma interferon (IFN-gamma) but more weakly and transiently by IFN-alpha. There are several putative kappa B motifs and numerous AA(G/A)G(G/T)A and GAAANN motifs throughout the promoter. The IRF-1 promoter is not autoregulated by the IRF-1 gene product. IFN inducibility of the promoter was studied with 5' deletion mutants linked to a heterologous reporter gene. Gel mobility shift assays were used to show IFN-inducible factor binding to the IRF-1 promoter. These studies showed that IFN inducibility is conferred by a novel imperfect inverted-repeat arrangement of two GAAANN motifs within a domain, 130 nucleotides upstream of transcription initiation. This inverted repeat binds a factor upon induction with IFN and can confer IFN inducibility on a heterologous promoter. Conversely, point mutations of the inverted repeat are not IFN inducible when linked to the same heterologous promoter.

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43

Sims, S. H., Y. Cha, M. F. Romine, P. Q. Gao, K. Gottlieb, and A. B. Deisseroth. "A novel interferon-inducible domain: structural and functional analysis of the human interferon regulatory factor 1 gene promoter." Molecular and Cellular Biology 13, no. 1 (January 1993): 690–702. http://dx.doi.org/10.1128/mcb.13.1.690.

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We have cloned and functionally characterized the human interferon regulatory factor 1 (IRF-1) gene promoter. The promoter contains a CpG island, with several GC boxes, a CAAT box, but no TATA box. IRF-1 mRNA is strongly induced by gamma interferon (IFN-gamma) but more weakly and transiently by IFN-alpha. There are several putative kappa B motifs and numerous AA(G/A)G(G/T)A and GAAANN motifs throughout the promoter. The IRF-1 promoter is not autoregulated by the IRF-1 gene product. IFN inducibility of the promoter was studied with 5' deletion mutants linked to a heterologous reporter gene. Gel mobility shift assays were used to show IFN-inducible factor binding to the IRF-1 promoter. These studies showed that IFN inducibility is conferred by a novel imperfect inverted-repeat arrangement of two GAAANN motifs within a domain, 130 nucleotides upstream of transcription initiation. This inverted repeat binds a factor upon induction with IFN and can confer IFN inducibility on a heterologous promoter. Conversely, point mutations of the inverted repeat are not IFN inducible when linked to the same heterologous promoter.

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44

Zuo, Kun, Chen Fang, Yuan Fu, Zheng Liu, Ye Liu, Lifeng Liu, Yuxing Wang, et al. "The Impact of Sleep Disturbance on Gut Microbiota, Atrial Substrate, and Atrial Fibrillation Inducibility in Mice: A Multi-Omics Analysis." Metabolites 12, no. 11 (November 20, 2022): 1144. http://dx.doi.org/10.3390/metabo12111144.

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This study examined the effect of sleep disturbance on gut microbiota (GM), atrial substrate, and atrial fibrillation (AF) inducibility. C57BL/6 mice were subjected to six weeks of sleep deprivation (SD) using the method of modified multiple-platform. Transesophageal burst pacing was performed to evaluate AF inducibility. Feces, plasma, and an atrium were collected and analyzed by 16s rRNA sequencing, liquid chromatography–mass spectrometry (LC-MS)-based metabolome, histological studies, and transcriptome. Higher AF inducibility (2/30 of control vs. 15/30 of SD, p = 0.001) and longer AF duration (p < 0.001), concomitant with aggravated fibrosis, collagen, and lipid accumulation, were seen in the SD mice compared to control mice. Meanwhile, elevated alpha diversity, higher abundance of Flavonifractor, Ruminococcus, and Alloprevotella, as well as imbalanced functional pathways, were observed in the gut of SD mice. Moreover, the global patterns for the plasma metabolome were altered, e.g., the decreased butanoate metabolism intermediates in SD mice. In addition, disrupted metabolic homeostasis in the SD atrium, such as fatty acid metabolism, was analyzed by the transcriptome. These results demonstrated that the crosstalk between GM and atrial metabolism might be a promising target for SD-mediated AF susceptibility.

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45

Santangeli, Pasquale, Erica S. Zado, Fermin C. Garcia, Michael P. Riley, David Lin, David S. Frankel, Gregory E. Supple, et al. "Lack of prognostic value of atrial arrhythmia inducibility and change in inducibility status after catheter ablation of atrial fibrillation." Heart Rhythm 15, no. 5 (May 2018): 660–65. http://dx.doi.org/10.1016/j.hrthm.2017.10.023.

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46

Rubio, MA, C. Lopez-Rodriguez, A. Nueda, P. Aller, AL Armesilla, MA Vega, and AL Corbi. "Granulocyte-macrophage colony-stimulating factor, phorbol ester, and sodium butyrate induce the CD11c integrin gene promoter activity during myeloid cell differentiation." Blood 86, no. 10 (November 15, 1995): 3715–24. http://dx.doi.org/10.1182/blood.v86.10.3715.bloodjournal86103715.

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To analyze the activity of the CD11c promoter during myeloid differentiation without the limitations of transient expression systems, we have stably transfected the myeloid U937 cell line with the pCD11C361-Luc plasmid, in which the expression of the firefly luciferase cDNA is driven by the CD11c promoter region -361/+43, previously shown to confer myeloid specificity to reporter genes. The stable transfectants (U937-C361) retained the ability to differentiate in response to phorbol-ester (PMA), sodium butyrate (SB), granulocyte- macrophage colony-stimulating factor (GM-CSF), and other differentiating agents. U937-C361 differentiation correlated with increased cellular luciferase levels, showing the inducibility of the CD11c promoter during myeloid differentiation and establishing the U937- C361 cells as a suitable system for studying the myeloid differentiation-inducing capacity of cytokines, growth, factors, and other biological response modifiers. Unexpectedly, the inducibility of the CD11c gene promoter showed distinct kinetics and magnitude on the PMA-, SB-, GM-CSF-triggered differentiation. Moreover, SB synergized with either PMA or GM-CSF in enhancing both the CD11c promoter activity and the cell surface expression of p150,95 on differentiating U937 cells. Furthermore, we showed the existence of a c-Myb-binding site at - 85, the importance of the -99/-61 region in the CD11c promoter inducibility during PMA- or SB-triggered differentiation, and the dependency of the GM-CSF and PMA responsiveness of the CD11c promoter on an intact AP-1-binding site located at -60. These results, together with the lack of functional effect of mutations disrupting the Sp1-and Myb-binding sites within the proximal region of the CD11c promoter, indicate that the myeloid differentiation pathways indicated by SB and phorbol esters (or GM-CSF) activate a distinct set of transcription factors and show that the myeloid differentiation-inducibility of the CD11c gene maps to the -99/-53 proximal region of the promoter.

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47

Rincon, M., and R. A. Flavell. "Regulation of AP-1 and NFAT transcription factors during thymic selection of T cells." Molecular and Cellular Biology 16, no. 3 (March 1996): 1074–84. http://dx.doi.org/10.1128/mcb.16.3.1074.

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The ability of thymocytes to express cytokine genes changes during the different stages of thymic development. Although CD4- CD8- thymocytes are able to produce a wide spectrum of cytokines in response to a T-cell receptor (TcR)-independent stimulus, as they approach the double-positive (DP) CD4+ CD8+ stage, they lose the ability to produce cytokine. After the DP stage, thymocytes become single-positive CD4+ or CD8+ thymocytes which reacquire the ability to secrete cytokines. In an attempt to understand the molecular basis of this specific regulatin, we use AP-1-luciferase and newly generated NFAT-luciferase transgenic mice to analyze the transcriptional and DNA-binding activities of these two transcription factors that are involved in the regulation of cytokine gene expression. Here, we show that both AP-1 and NFAT transcriptional activities are not inducible in the majority of DP cells but that during the differentiation of DP cells to the mature single-positive stage, thymocytes regain this inducibility. Subpopulation analysis demonstrates that this inducibility is reacquired at the DP stage before the down-modulation of one of the coreceptors. Indeed AP-1 inducibility, just like the ability to express the interleukin-2 gene, is reacquired during the differentiation of DP TcRlow CD69low heat-stable antigen (HSA)high thymocytes to DP TcRhigh CD69high HSAhigh cells, which is considered to be the consequence of the first signal that initiates positive selection. We therefore propose that the inability of DP thymocytes to induce AP-1 and NFAT activities is one of the causes for the lack of cytokine gene expression at this stage and that this inducibility is reacquired at the latest stage of DP differentiation as a consequence of positive selection. This could be a mechanism to prevent the activation of DP thymocytes before selection has taken place.

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48

Lindert, Uschi, Mirjam Cramer, Michael Meuli, Oleg Georgiev, and Walter Schaffner. "Metal-Responsive Transcription Factor 1 (MTF-1) Activity Is Regulated by a Nonconventional Nuclear Localization Signal and a Metal-Responsive Transactivation Domain." Molecular and Cellular Biology 29, no. 23 (September 21, 2009): 6283–93. http://dx.doi.org/10.1128/mcb.00847-09.

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ABSTRACT Metal-responsive transcription factor 1 (MTF-1) mediates both basal and heavy metal-induced transcription of metallothionein genes and also regulates other genes involved in the cell stress response and in metal homeostasis. In resting cells, MTF-1 localizes to both the cytoplasm and the nucleus but quantitatively accumulates in the nucleus upon metal load and under other stress conditions. Here we show that within the DNA-binding domain, a region spanning zinc fingers 1 to 3 (amino acids [aa] 137 to 228 in human MTF-1) harbors a nonconventional nuclear localization signal. This protein segment confers constitutive nuclear localization to a cytoplasmic marker protein. The deletion of the three zinc fingers impairs nuclear localization. The export of MTF-1 to the cytoplasm is controlled by a classical nuclear export signal (NES) embedded in the acidic activation domain. We show that this activation domain confers metal inducibility in distinct cell types when fused to a heterologous DNA-binding domain. Furthermore, the cause of a previously described stronger inducibility of human versus mouse MTF-1 could be narrowed down to a 3-aa difference in the NES; “humanizing” mouse MTF-1 at these three positions enhanced its metal inducibility to the level of human MTF-1.

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49

Winterhalter, Wade E., and Kenneth M. Fedorka. "Sex-specific variation in the emphasis, inducibility and timing of the post-mating immune response in Drosophila melanogaster." Proceedings of the Royal Society B: Biological Sciences 276, no. 1659 (December 9, 2008): 1109–17. http://dx.doi.org/10.1098/rspb.2008.1559.

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Ecological immunology attempts to explain variation in immune function. Much of this work makes predictions about how potential hosts should invest in overall immunity. However, this ‘overall’ perspective under-emphasizes other critical aspects, such as the specificity, inducibility and timing of an immune response. Here, we investigate these aspects by examining gene regulation across several immune system components in both male and female Drosophila melanogaster prior to and after mating. To elucidate potentially important temporal dynamics, we also assayed several genes over time. We found that males and females emphasized different components of their immune system, however overall investment was similar. Specifically, the sexes emphasized different gene paralogues within major gene families, and males tended to invest more in gram-negative defence. By contrast, the inducibility of the immune response was both transient (lasting approx. 24 hours) and equal between the sexes. Furthermore, mating tended to induce humoral gene upregulation, while cell-mediated genes were unaffected. Within the humoral system, gram-negative bacterial defence genes exhibited a greater inducibility than those associated with fungal or gram-positive bacterial defence. Our results suggest that variation in the effectiveness of the immune response between the sexes may be driven by differences in emphasis rather than overall investment.

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Hulla, J. E., and M. R. Juchau. "Developmental Aspects of P450iiia: Prenatal Activity and Inducibility." Drug Metabolism Reviews 20, no. 2-4 (January 1989): 765–79. http://dx.doi.org/10.3109/03602538909103577.

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Journal articles on the topic 'Inducibility'

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