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Artykuły w czasopismach na temat „TGIFLX”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Ousati Ashtiani, Z., M. Ayati, M. H. Modarresi, et al. "Association of TGIFLX/Y mRNA expression with prostate cancer." Medical Oncology 26, no. 1 (2008): 73–77. http://dx.doi.org/10.1007/s12032-008-9086-7.

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Aarabi, M., Z. Ousati-Ashtiani, A. Nazarian, M. H. Modarressi, and M. Heidari. "Association of TGIFLX/Y mRNA expression with azoospermia in infertile men." Molecular Reproduction and Development 75, no. 12 (2008): 1761–66. http://dx.doi.org/10.1002/mrd.20906.

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Konrad, Christian, Ronald C. Wek, and William J. Sullivan. "A GCN2-Like Eukaryotic Initiation Factor 2 Kinase Increases the Viability of Extracellular Toxoplasma gondii Parasites." Eukaryotic Cell 10, no. 11 (2011): 1403–12. http://dx.doi.org/10.1128/ec.05117-11.

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ABSTRACT Toxoplasmosis is a significant opportunistic infection caused by the protozoan parasite Toxoplasma gondii , an obligate intracellular pathogen that relies on host cell nutrients for parasite proliferation. Toxoplasma parasites divide until they rupture the host cell, at which point the extracellular parasites must survive until they find a new host cell. Recent studies have indicated that phosphorylation of Toxoplasma eukaryotic translation initiation factor 2-alpha (TgIF2α) plays a key role in promoting parasite viability during times of extracellular stress. Here we report the cloni

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4

Raoofian, Reza. "Impact of TGIFLX Expression on the Regulation of BCL2 and BAX in Prostate Cancer Cell Line (LNCaP)." British Journal of Medicine and Medical Research 3, no. 4 (2013): 953–61. http://dx.doi.org/10.9734/bjmmr/2013/2904.

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SULLIVAN, William J., Jana NARASIMHAN, Micah M. BHATTI, and Ronald C. WEK. "Parasite-specific eIF2 (eukaryotic initiation factor-2) kinase required for stress-induced translation control." Biochemical Journal 380, no. 2 (2004): 523–31. http://dx.doi.org/10.1042/bj20040262.

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The ubiquitous intracellular parasite Toxoplasma gondii (phylum Apicomplexa) differentiates into an encysted form (bradyzoite) that can repeatedly re-emerge as a life-threatening acute infection (tachyzoite) upon impairment of immunity. Since the switch from tachyzoite to bradyzoite is a stress-induced response, we sought to identify components related to the phosphorylation of the α subunit of eIF2 (eukaryotic initiation factor-2), a well-characterized event associated with stress remediation in other eukaryotic systems. In addition to characterizing Toxoplasma eIF2α (TgIF2α), we have discove

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6

Hamid, Rizwan, and Stephen J. Brandt. "TG-Interacting Factor Regulates Proliferation and Differentiation of Human Myeloid Leukemia Cells." Blood 112, no. 11 (2008): 4731. http://dx.doi.org/10.1182/blood.v112.11.4731.4731.

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Abstract Transforming growth-interacting factor (TGIF) is a homeobox transcriptional repressor that has been implicated in holoprosencephaly and various types of cancer. TGIF is expressed in hematopoietic stem cells and modulates TGF-β and retinoic acid (RA) signaling, both of which play an important role in hematopoiesis. We recently reported that TGIF’s levels correlate inversely with survival in patients with acute myelogenous leukemia. Here we present the first direct evidence of a role for TGIF in myelopoiesis. We used short hairpin RNA interference to define the effects of TGIF knockdown

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7

Hyman, Cathy A., Laurent Bartholin, Stuart J. Newfeld, and David Wotton. "DrosophilaTGIF Proteins Are TranscriptionalActivators." Molecular and Cellular Biology 23, no. 24 (2003): 9262–74. http://dx.doi.org/10.1128/mcb.23.24.9262-9274.2003.

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ABSTRACT The information carried by transforming growth factor β (TGF-β) signaling molecules induces profound responses in target cells. To restrict this information to appropriate cells, TGF-β signaling pathways are tightly regulated by dynamic interactions with transcriptional activators and repressors. Numerous cross-species experiments have shown that TGF-β family members and their signal transduction machinery (receptors and Smad signal transducers) are functionally conserved between vertebrates and invertebrates. TG-interacting factor (TGIF) is a homeodomain-containing transcriptional co

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8

Melhuish, Tiffany A., Kenichiro Taniguchi, and David Wotton. "Tgif1 and Tgif2 Regulate Axial Patterning in Mouse." PLOS ONE 11, no. 5 (2016): e0155837. http://dx.doi.org/10.1371/journal.pone.0155837.

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Shen, Jun, and Christopher A. Walsh. "Targeted Disruption of Tgif, the Mouse Ortholog of a Human Holoprosencephaly Gene, Does Not Result in Holoprosencephaly in Mice." Molecular and Cellular Biology 25, no. 9 (2005): 3639–47. http://dx.doi.org/10.1128/mcb.25.9.3639-3647.2005.

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ABSTRACT 5′-TG-3′-interacting factor or transforming growth factor beta (TGF-β)-induced factor (TGIF) belongs to a family of evolutionarily conserved proteins that are characterized by an atypical three-amino-acid loop extension homeodomain. In vitro studies have implicated TGIF as a transcriptional repressor and corepressor in retinoid and TGF-β signaling pathways that regulate several important biological processes. Heterozygous nonsense and missense mutations of the human TGIF gene have been associated with holoprosencephaly, the most common congenital malformation of the forebrain. In mice

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10

Powers, Shannon E., Kenichiro Taniguchi, Weiwei Yen, et al. "Tgif1 and Tgif2 regulate Nodal signaling and are required for gastrulation." Development 137, no. 2 (2009): 249–59. http://dx.doi.org/10.1242/dev.040782.

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Taniguchi, Kenichiro, Shannon E. Powers, and David Wotton. "The role of Tgif and Tgif2 during head development." Developmental Biology 331, no. 2 (2009): 525. http://dx.doi.org/10.1016/j.ydbio.2009.05.516.

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12

He, Xiaoling, Yao Nie, Heng Zhou, et al. "Structural Insight into the Binding of TGIF1 to SIN3A PAH2 Domain through a C-Terminal Amphipathic Helix." International Journal of Molecular Sciences 22, no. 23 (2021): 12631. http://dx.doi.org/10.3390/ijms222312631.

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TGIF1 is a transcriptional repressor playing crucial roles in human development and function and is associated with holoprosencephaly and various cancers. TGIF1-directed transcriptional repression of specific genes depends on the recruitment of corepressor SIN3A. However, to date, the exact region of TGIF1 binding to SIN3A was not clear, and the structural basis for the binding was unknown. Here, we demonstrate that TGIF1 utilizes a C-terminal domain (termed as SIN3A-interacting domain, SID) to bind with SIN3A PAH2. The TGIF1 SID adopts a disordered structure at the apo state but forms an amph

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13

Guo, Xiaobo, Gang Li, Yufeng Zhao, and Bo Zhao. "TGFB Induced Factor Homeobox 2 Induces Deterioration of Bladder Carcinoma via Activating CD2 Cytoplasmic Tail Binding Protein 2." Journal of Biomedical Nanotechnology 19, no. 9 (2023): 1670–76. http://dx.doi.org/10.1166/jbn.2023.3657.

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Bladder carcinoma is a complex and aggressive malignancy with limited treatment options. In this study, we aimed to investigate the expression pattern of TGIF2 in bladder carcinoma and its clinical significance, as well as its functional role and interaction with CD2BP2 in disease progression. Through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis, we found that TGIF2 was highly expressed in bladder carcinoma tissues compared to normal bladder mucosa. Furthermore, elevated TGIF2 levels were associated with advanced tumor stage and larger tumor size, indicating

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14

Chen, Liyang, Chaoyin Jiang, Shashi Ranjan Tiwari, et al. "TGIF1 Gene Silencing in Tendon-Derived Stem Cells Improves the Tendon-to-Bone Insertion Site Regeneration." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2101–14. http://dx.doi.org/10.1159/000438568.

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Background/Aims: The slow healing process of tendon-to-bone junctions can be accelerated via implanted tendon-derived stem cells (TDSCs) with silenced transforming growth interacting factor 1 (TGIF1) gene. Tendon-to-bone insertion site is the special form of connective tissues derivatives of common connective progenitors, where TGF-β plays bidirectional effects (chondrogenic or fibrogenic) through different signaling pathways at different stages. A recent study revealed that TGF-β directly induces the chondrogenic gene Sox9. However, TGIF1 represses the expression of the cartilage master Sox9

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15

Peng, Wu-Xun, Chuan Ye, Wen-Tao Dong, et al. "MicroRNA-34a alleviates steroid-induced avascular necrosis of femoral head by targeting Tgif2 through OPG/RANK/RANKL signaling pathway." Experimental Biology and Medicine 242, no. 12 (2017): 1234–43. http://dx.doi.org/10.1177/1535370217703975.

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The study aims to investigate the effect of microRNA-34a (miR-34a) targeting Tgif2 on steroid-induced avascular necrosis of femoral head (SANFH) by regulating OPG/RANK/RANKL signaling pathway. SD rats were divided into normal control and model (RNAKL rat models) groups. The model group was further assigned into model control, negative control, miR-34a mimics and miR-34a inhibitors groups. QRT-PCR was applied to detect miR-34a, Tgif2, OPG, RANK and RNAKL mRNA expressions. Femoral head tissues were collected for Micro-CT scanning and HE staining. QRT-PCR and Western blotting were used to detect

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Shao, Yuefeng, Xinya Hu, and Xuejian Wu. "LncRNA X inactive-specific transcript promotes osteoclast differentiation through Tgif2 by acting as a ceRNA of miR-590-3p in a murine model." Regenerative Medicine 16, no. 7 (2021): 643–53. http://dx.doi.org/10.2217/rme-2020-0174.

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Aim: This study aims to investigate whether long noncoding RNA (lncRNA) X-inactive specific transcript (Xist) can regulate osteoclast differentiation in osteoporosis and the mechanism. Materials & methods: The mouse model of osteoporosis was established by ovariectomy surgery. Osteoclast differentiation from RAW264.7 cells was induced in vitro. The relationships between associated genes were assessed. Results: Xist and Tgif2 were upregulated, but miR-590-3p was downregulated in ovariectomy mouse femurs and cell models. Xist knockdown or miR-590-3p overexpression inhibited Tgif2 expression

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Bai, Fuyan, Liping Zheng, Li Tao, Shikai Wang, Yuchen Li, and Lijun Hou. "Mechanism of TGIF1 on glycolipid metabolism disorders in mice with type 2 diabetes." BMJ Open Diabetes Research & Care 13, no. 1 (2025): e004509. https://doi.org/10.1136/bmjdrc-2024-004509.

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IntroductionType 2 diabetes (T2D) is a chronic condition characterized by high levels of blood glucose resulting from the inefficiency of insulin. This study aims to explore the mechanism of TGFB-induced factor homeobox 1 (TGIF1) in the glycolipid metabolism of mice with T2D.Research design and methodsMice with T2D were induced by high-fat diet and low-dose streptozotocin (STZ) injection. After TGIF1 was overexpressed in mice with T2D, the weight was monitored. The levels of fasting plasma glucose, fasting serum insulin, triglycerides, total cholesterol, low-density lipoprotein cholesterol, an

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Verrotti, Alberto, Chiara Palka, Giovanni Prezioso, et al. "Deletion 18p11.32p11.31 in a Child with Global Developmental Delay and Atypical, Drug-Resistant Absence Seizures." Cytogenetic and Genome Research 146, no. 2 (2015): 115–19. http://dx.doi.org/10.1159/000438502.

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We report the first case of an 18p11.32 deletion, detected by array CGH, associated with a drug-resistant form of atypical absence epilepsy, global developmental delay and no signs of holoprosencephaly (HPE). In particular, this region encompasses 19 genes, and none of these genes have been strictly associated with epilepsy. Among these, TGIF1 is expressed in the fetal and adult nervous system, and its deletion has been related to central nervous system diseases. TGIF1 deletions have previously been reported in patients with a comparable phenotype as seen in our case and in children whose neur

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19

Qiao, Jialu, Qian Peng, Feng Qian, et al. "HIV-1 Vpr protein upregulates microRNA-210-5p expression to induce G2 arrest by targeting TGIF2." PLOS ONE 16, no. 12 (2021): e0261971. http://dx.doi.org/10.1371/journal.pone.0261971.

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MicroRNAs (miRNAs) are important molecules that mediate virus-host interactions, mainly by regulating gene expression via gene silencing. Here, we demonstrated that HIV-1 infection upregulated miR-210-5p in HIV-1-inoculated cell lines and in the serum of HIV-1-infected individuals. Luciferase reporter assays and western blotting confirmed that a target protein of miR-210-5p, TGIF2, is regulated by HIV-1 infection. Furthermore, HIV-1 Vpr protein induced miR-210-5p expression. The use of a miR-210-5p inhibitor and TGIF2 overexpression showed that Vpr upregulated miR-210-5p and thereby downregula

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Eshetu, Dereje, Mulugeta Atnafu, and Mulugeta Woldemichael. "Technology integrated guided inquiry-based learning approach and pre-service mathematics teachers’ attitude towards learning geometry." Mediterranean Journal of Social & Behavioral Research 7, no. 1 (2023): 3–13. http://dx.doi.org/10.30935/mjosbr/12560.

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The study investigated the effects of technology-integrated guided inquiry (TGIBL), guided inquiry (GIBL), and traditional (TRAD) strategies on pre-service mathematics teachers’ attitudes towards geometry in college of teacher educations. The study employed nonequivalent quasi-experimental design with two experimental groups and control group. A three-stage sampling method was used. The experimental groups were exposed to TGIBL (n=48) and GIBL (n=38), while comparison group (n=30) with TRAD approach. The geometry attitude scale (GAS) questionnaire was the instrument employed to collect data fr

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Nakaguma, Marilena, Nathalia Garcia Bianchi Pereira Ferreira, Anna Flavia Figueredo Benedetti, et al. "Allelic Variants in Established Hypopituitarism Genes Expand Our Knowledge of the Phenotypic Spectrum." Genes 12, no. 8 (2021): 1128. http://dx.doi.org/10.3390/genes12081128.

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We report four allelic variants (three novel) in three genes previously established as causal for hypopituitarism or related disorders. A novel homozygous variant in the growth hormone gene, GH1 c.171delT (p.Phe 57Leufs*43), was found in a male patient with severe isolated growth hormone deficiency (IGHD) born to consanguineous parents. A hemizygous SOX3 allelic variant (p.Met304Ile) was found in a male patient with IGHD and hypoplastic anterior pituitary. YASARA, a tool to evaluate protein stability, suggests that p.Met304Ile destabilizes the SOX3 protein (ΔΔG = 2.49 kcal/mol). A rare, hetero

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Bartholin, Laurent, Shannon E. Powers, Tiffany A. Melhuish, Samuel Lasse, Michael Weinstein, and David Wotton. "TGIF Inhibits Retinoid Signaling." Molecular and Cellular Biology 26, no. 3 (2006): 990–1001. http://dx.doi.org/10.1128/mcb.26.3.990-1001.2006.

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ABSTRACT TGIF (TG-interacting factor) represses transforming growth factor β (TGF-β)-activated gene expression and can repress transcription via a specific retinoid response element. Mutations in human TGIF are associated with holoprosencephaly, a severe defect of craniofacial development with both genetic and environmental causes. Both TGF-β and retinoic acid signaling are implicated in craniofacial development. Here, we analyze the role of TGIF in regulating retinoid responsive gene expression. We demonstrate that TGIF interacts with the ligand binding domain of the RXRα retinoid receptor an

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Gunatillake, Tilini, Hannah E. J. Yong, Caroline E. Dunk, et al. "Homeobox gene TGIF-1 is increased in placental endothelial cells of human fetal growth restriction." Reproduction 152, no. 5 (2016): 457–65. http://dx.doi.org/10.1530/rep-16-0068.

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Aberrant placental angiogenesis is associated with fetal growth restriction (FGR). In mice, targeted disruption of the homeobox gene, transforming growth β-induced factor (Tgif-1), which is also a transcription factor, causes defective placental vascularisation. Nevertheless, the role of TGIF-1 in human placental angiogenesis is unclear. We have previously reported increased TGIF-1 expression in human FGR placentae and demonstrated localisation of TGIF-1 protein in placental endothelial cells (ECs). However, its functional role remains to be investigated. In this study, we aimed to specificall

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Claudia Burbank. "TGIF." Antioch Review 70, no. 4 (2012): 727. http://dx.doi.org/10.7723/antiochreview.70.4.0727.

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Yang, Shenghong, Matthew A. Nugent та Mikhail P. Panchenko. "EGF antagonizes TGF-β-induced tropoelastin expression in lung fibroblasts via stabilization of Smad corepressor TGIF". American Journal of Physiology-Lung Cellular and Molecular Physiology 295, № 1 (2008): L143—L151. http://dx.doi.org/10.1152/ajplung.00289.2007.

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We previously reported that neutrophil elastase (NE) downregulates transforming growth factor-β (TGF-β)-maintained tropoelastin mRNA levels in lung fibroblasts through transactivation of the epidermal growth factor (EGF) receptor (EGFR)/Mek/Erk pathway, which is dependent on the NE-initiated release of soluble EGFR ligands. In the present study, we investigated the mechanism by which EGF downregulates tropoelastin expression. We found that EGF downregulates tropoelastin expression through inhibition of TGF-β signaling. We show that EGF does not prevent the TGF-β-induced nuclear accumulation of

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Murthi, P., N. Pathirage, A. Borg, S. Brennecke, and B. Kalionis. "205. Homeobox gene TGIF is increased in human idiopathic fetal growth restriction." Reproduction, Fertility and Development 20, no. 9 (2008): 5. http://dx.doi.org/10.1071/srb08abs205.

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Fetal Growth Restriction (FGR) is a clinically significant pregnancy disorder in which the fetus fails to achieve its full growth potential in utero. Recently, we identified a novel homeobox gene TGIF, in the placenta using microarray expression profiling (1). Targeted mutation of tgif in mouse results in placental dysfunction (2). In this study, we have investigated TGIF expression levels in idiopathic FGR. FGR-affected placental samples were collected based on strict clinical criteria to ensure inclusion of cases at the severe end of the spectrum of the disease. TGIF mRNA expression was anal

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Mar, Lynn, and Pamela A. Hoodless. "Embryonic Fibroblasts from Mice Lacking Tgif Were Defective in Cell Cycling." Molecular and Cellular Biology 26, no. 11 (2006): 4302–10. http://dx.doi.org/10.1128/mcb.02156-05.

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ABSTRACT Holoprosencephaly (HPE) is the most common structural anomaly of the human brain, resulting from incomplete cleavage of the developing forebrain during embryogenesis. Haploinsufficient mutations in the TG-interacting factor (TGIF) gene were previously identified in a subset of HPE families and sporadic patients, and this gene is located within a region of chromosome 18 that is associated with nonrandom chromosomal aberrations in HPE patients. TGIF is a three-amino-acid loop extension (TALE) homeodomain-containing transcription factor that functions both as a corepressor of the transfo

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CHEN, Feifei, Kenji OGAWA, Raman P. NAGARAJAN, Meiyu ZHANG, Chenzhong KUANG, and Yan CHEN. "Regulation of TG-interacting factor by transforming growth factor-beta." Biochemical Journal 371, no. 2 (2003): 257–63. http://dx.doi.org/10.1042/bj20030095.

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TG-interacting factor (TGIF) is a transcriptional co-repressor that directly associates with Smad (Sma- and Mad-related protein) proteins and inhibits Smad-mediated transcriptional activation. By using Affymetrix (Santa Clara, CA, U.S.A.) oligonucleotide microarray analysis, we found that TGIF mRNA level was elevated by transforming-growth-factor-β (TGF-β) treatment in a human T-cell line, HuT78. Subsequent reverse-transcription PCR assays indicated that TGF-β1 and activin were able to induce a rapid and transient increase in the level of TGIF in both HuT78 and HepG2 hepatoma cells. To analyse

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Yan, Ling, Bethany Womack, Stephen J. Brandt, and Rizwan Hamid. "Transforming Growth-Interacting Factor (TGIF) Modulates Hematopoietic Stem Cell Functions." Blood 118, no. 21 (2011): 1279. http://dx.doi.org/10.1182/blood.v118.21.1279.1279.

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Abstract Abstract 1279 We have shown that quantitative expression of the stem cell expressed Transforming-growth-interfering factor (TGIF) is a predictor of patient survival in acute myelogenous leukemia (AML). By Kaplan-Meier analysis, patients whose leukemic cells expressed decreased levels of TGIF RNA had a mean survival of 12 months, while patients whose leukemic cells expressed TGIF at a higher level had a mean survival of 60 months (p=0.00001). TGIF is a homeobox transcriptional repressor and although it has been implicated in holoprosencephaly (HPE), whether it has a direct role in hema

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Hamid, Rizwan, Cindy L. Vnencak-Jones, Danko Martincic, Julie A. Means-Powell, Joy D. Cogan, and Stephen J. Brandt. "Recurrent Abnormalities in TGIF RNA Sequence in Blasts from Patients with Acute Myeloid Leukemia." Blood 104, no. 11 (2004): 419. http://dx.doi.org/10.1182/blood.v104.11.419.419.

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Abstract To identify genes with prognostic potential in acute myeloid leukemia (AML), we applied microarray analysis and real-time PCR to RNA from cryopreserved bone marrow or venous blood samples from 61 patients with newly diagnosed or relapsed AML, and the expression of one gene, TG-interacting factor (TGIF) was found to be highly predictive of relapse and survival. TGIF is a transcriptional repressor belonging to the TALE (three amino acid loop extension) class of homeobox proteins, and deletion or mutation of a single allele of TGIF is associated with the craniofacial genetic disorder hol

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Liu, Zi-Miao, Joseph T. Tseng, Duang-Yang Hong, and Huei-Sheng Huang. "Suppression of TG-interacting factor sensitizes arsenic trioxide-induced apoptosis in human hepatocellular carcinoma cells." Biochemical Journal 438, no. 2 (2011): 349–58. http://dx.doi.org/10.1042/bj20101653.

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HCC (hepatocellular carcinoma) is among the most common and lethal cancers worldwide with a poor prognosis mainly due to a high recurrence rate and chemotherapy resistance. ATO (arsenic trioxide) is a multi-target drug that has been effectively used as an anticancer drug in acute promyelocytic leukaemia. However, a Phase II trial involving patients with HCC indicates that the use of arsenic as a single agent is not effective against HCC. TGIF (TG-interacting factor) is a transcriptional co-repressor that interferes with TGF-β (transforming growth factor-β) signalling which plays a growth-inhib

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Ueberroth, Benjamin Edward, Hannah Ruth Robinson, S. Lindsey Davis, et al. "Molecular and clinical profiling of gastroenteropancreatic (GEP) neuroendocrine tumors (NETs): An analysis of the Oncology Research Information Exchange Network database." Journal of Clinical Oncology 43, no. 4_suppl (2025): 669. https://doi.org/10.1200/jco.2025.43.4_suppl.669.

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669 Background: The incidence of neuroendocrine tumors (NETs) is approximately 7 per 100,000 persons and rising. By location, tumors in the gastroenteropancreatic (GEP) region, particularly midgut NETs, are most common. The Oncology Research Information Exchange Network (ORIEN) database contains complementary clinical, genomic, and transcriptomic profiling, providing opportunities to identify novel associations between molecular features and clinical outcomes in GEP-NETs. Methods: Survival analyses were performed using the log-rank testing, and clinical features were evaluated using Wilcoxon a

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Shchekotikhin, Andrey E., Helen M. Treshalina, Michael I. Treshchalin, Eleonora R. Pereverzeva, Helen B. Isakova, and Alexander S. Tikhomirov. "Experimental Evaluation of Anticancer Efficiency and Acute Toxicity of Anthrafuran for Oral Administration." Pharmaceuticals 13, no. 5 (2020): 81. http://dx.doi.org/10.3390/ph13050081.

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The new antitumor agent anthrafuran has demonstrated a consistent effect in murine tumor models when administered parenterally due to the simultaneous inhibition of multiple cellular targets such as topoisomerases I/II and protein kinases. In this study, we assessed the anticancer efficiency and acute toxicity of anthrafuran administered orally. The action of anthrafuran was studied on transplanted tumor models which included P388 leukemia, Ca755 mammary adenocarcinoma, LLC lung carcinoma, and T47D human breast cancer xenografts on Balb/c nude mice. A significant antitumor efficacy of oral ant

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Kannappan, Sunand, Mehul Gupa, SungMyung Kang, et al. "ATRT-09. IDENTIFICATION OF POTENTIAL GENETIC DRIVERS OF METHOTREXATE (MTX) RESISTANCE IN ATYPICAL TERATOID RHABDOID TUMOURS (ATRT) THROUGH A GENOME-WIDE RNAI SCREEN." Neuro-Oncology 23, Supplement_1 (2021): i3. http://dx.doi.org/10.1093/neuonc/noab090.008.

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Abstract ATRT of the CNS constitute a group of rare and aggressive early childhood tumors with poor prognosis. While there are differing chemotherapeutic regimens for ATRT, high-dose MTX is a crucial component of many therapeutic protocols. Currently, the biological mechanisms contributing to the generation of MTX resistance in ATRT are unknown. To identify genes involved in MTX resistance in ATRT, an unbiased genome-wide RNAi screen on ATRT cell lines was conducted using 24,000 distinct shRNAs covering 8,000 genes. ATRT cells were transfected with a retrovirus containing pRS-shRNA vectors and

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Chen, Si, Lin Tao, Xiaoyun He, Ran Di, Xiangyu Wang, and Mingxing Chu. "Single-nucleotide polymorphisms in <i>FLT3</i>, <i>NLRP5</i>, and <i>TGIF1</i> are associated with litter size in Small-tailed Han sheep." Archives Animal Breeding 64, no. 2 (2021): 475–86. http://dx.doi.org/10.5194/aab-64-475-2021.

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Abstract. Previous studies have indicated that FLT3, NLRP5, and TGIF1 play a pivotal role in sheep fecundity. Nevertheless, little is known about the association of the polymorphisms of these genes with litter size (LS). In this study, the selected single-nucleotide polymorphisms (SNPs) were genotyped using a Sequenom MassARRAY® platform, and the distribution of different genotypes of the SNPs in the seven sheep breeds (Small-tailed Han, Hu, Cele Black, Suffolk, Tan, Prairie Tibetan, and Sunite sheep) were analyzed. The reliability of the estimated allele frequency for all seven SNPs was at le

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Hamid, Rizwan, Johnequia Patterson, Danko Martincic, and Stephen J. Brandt. "Complex Regulation of the Homeobox Transcription Factor TGIF: Differential Expression of Multiple 5′ Isoforms." Blood 106, no. 11 (2005): 4254. http://dx.doi.org/10.1182/blood.v106.11.4254.4254.

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Abstract TG-interacting factor (TGIF) is a transcriptional repressor belonging to the TALE (three amino acid loop extension) class of homeobox proteins. In addition to its involvement by mutation or deletion in the inherited craniofacial disorder holoprosencephaly, we have shown that expression of TGIF is highly predictive of relapse and survival in acute myelogenous leukemia (AML). To better understand how TGIF expression is regulated, we characterized its genomic structure using expressed sequence tag analysis, reverse transcriptase-coupled PCR, and rapid amplification of cDNA ends. These st

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Mobini, Gholam Reza, Arefeh Ghafari, Saeid Amanpour, et al. "In vivo identification of novel TGIF2LX target genes in colorectal adenocarcinoma using the cDNA-AFLP method." Arab Journal of Gastroenterology 19, no. 2 (2018): 65–70. http://dx.doi.org/10.1016/j.ajg.2018.05.001.

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Melhuish, Tiffany A., David D. Chung, Glen A. Bjerke, and David Wotton. "Tgif1 represses apolipoprotein gene expression in liver." Journal of Cellular Biochemistry 111, no. 2 (2010): 380–90. http://dx.doi.org/10.1002/jcb.22713.

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Razzaque, Mohammed S., and Azeddine Atfi. "TGIF1-Twist1 axis in pancreatic ductal adenocarcinoma." Computational and Structural Biotechnology Journal 18 (2020): 2568–72. http://dx.doi.org/10.1016/j.csbj.2020.09.023.

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Dereje, Eshetu Wordofe, Atnafu Mulugeta, and Woldemichael Mulugeta. "Pre-service mathematics teachers’ geometric reasoning skills with technology-integrated guided inquiry approach." Pedagogical Research 8, no. 4 (2023): em0164. http://dx.doi.org/10.29333/pr/13332.

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This study was intended to examine the progress of the geometric reasoning skills of pre-service mathematics teachers (PSMTs) in the College of Teacher Education, Oromiya, Ethiopia. In the study, there were three different classes: EG1 (n=48), EG2 (n=38), and CG (n=30), where PSMTs in EG1 were treated with technology into guided inquiry-based learning (TGIBL), EG2 with guided inquiry-based learning (GIBL), and CG with a conventional learning approach. A geometric reasoning test was used to collect data. The data were analyzed using a one-way ANOVA and a paired sample t-test. The findings showe

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Li, Rong, Xuejing Xu, Shuo Gao, et al. "Circular RNA CDR1as Mediated by Human Antigen R (HuR) Promotes Gastric Cancer Growth via miR-299-3p/TGIF1 Axis." Cancers 15, no. 23 (2023): 5556. http://dx.doi.org/10.3390/cancers15235556.

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Background: Gastric cancer (GC) remains a common malignancy worldwide with a limited understanding of the disease mechanisms. A novel circular RNA CDR1as has been recently reported to be a crucial regulator of human cancer. However, its biological role and mechanism in the GC growth are still far from clear. Methods: Small interfering RNAs (siRNAs), lentivirus or plasmid vectors were applied for gene manipulation. The CDR1as effects on the GC growth were evaluated in CCK8 and colony formation assays, a flow cytometry analysis and mouse xenograft tumor models. A bioinformatics analysis combined

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Chou, Ming-Yung, Pei-Ling Hsieh, Shih-Chi Chao, Yi-Wen Liao, Cheng-Chia Yu, and Chang-Yi Tsai. "MiR-424/TGIF2-Mediated Pro-Fibrogenic Responses in Oral Submucous Fibrosis." International Journal of Molecular Sciences 24, no. 6 (2023): 5811. http://dx.doi.org/10.3390/ijms24065811.

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Oral submucous fibrosis (OSF) has been recognized as a potentially malignant disorder and is characterized by inflammation and the deposition of collagen. Among various regulators of fibrogenesis, microRNAs (miR) have received great attention but the detailed mechanisms underlying the miR-mediated modulations remain largely unknown. Here, we showed that miR-424 was aberrantly overexpressed in OSF tissues, and then we assessed its functional role in the maintenance of myofibroblast characteristics. Our results demonstrated that the suppression of miR-424 markedly reduced various myofibroblast a

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Kerr, Tyler C., Tawny N. Cuykendall, Laura C. Luettjohann, and Douglas W. Houston. "Maternal Tgif1 regulates nodal gene expression in Xenopus." Developmental Dynamics 237, no. 10 (2008): 2862–73. http://dx.doi.org/10.1002/dvdy.21707.

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Epstein, Scott K. "TGIF: Tracheal Gas Insufflation." Chest 122, no. 5 (2002): 1515–17. http://dx.doi.org/10.1378/chest.122.5.1515.

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Tsymbal, Dariia O., Dmytro O. Minchenko, Olena O. Khita, et al. "ERN1 knockdown modifies the effect of glucose deprivation on homeobox gene expressions in U87 glioma cells." Endocrine Regulations 54, no. 3 (2020): 196–206. http://dx.doi.org/10.2478/enr-2020-0022.

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AbstractObjective. The aim of the present investigation was to study the expression of genes encoding homeobox proteins ZEB2 (zinc finger E-box binding homeobox 2), TGIF1 (TGFB induced factor homeobox 1), SPAG4 (sperm associated antigen 4), LHX1 (LIM homeobox 1), LHX2, LHX6, NKX3-1 (NK3 homeobox 1), and PRRX1 (paired related homeobox 1) in U87 glioma cells in response to glucose deprivation in control glioma cells and cells with knockdown of ERN1 (endoplasmic reticulum to nucleus signaling 1), the major pathway of the endoplasmic reticulum stress signaling, for evaluation of it possible signif

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Al-Rabadi, Anas. "An extended Green-Sasao hierarchy of canonical ternary Galois forms and Universal Logic Modules." Facta universitatis - series: Electronics and Energetics 30, no. 1 (2017): 49–66. http://dx.doi.org/10.2298/fuee1701049a.

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A new extended Green-Sasao hierarchy of families and forms with a new sub-family for many-valued Reed-Muller logic is introduced. Recently, two families of binary canonical Reed-Muller forms, called Inclusive Forms (IFs) and Generalized Inclusive Forms (GIFs) have been proposed, where the second family was the first to include all minimum Exclusive Sum-Of-Products (ESOPs). In this paper, we propose, analogously to the binary case, two general families of canonical ternary Reed-Muller forms, called Ternary Inclusive Forms (TIFs) and their generalization of Ternary Generalized Inclusive Forms (T

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Dinsmore, Colin J., and Philippe Soriano. "A Fateful Decision: Tgif1 and Cardiac Neural Crest Identity." Developmental Cell 53, no. 3 (2020): 255–56. http://dx.doi.org/10.1016/j.devcel.2020.04.013.

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Melhuish, Tiffany A., Christopher M. Gallo, and David Wotton. "TGIF2 Interacts with Histone Deacetylase 1 and Represses Transcription." Journal of Biological Chemistry 276, no. 34 (2001): 32109–14. http://dx.doi.org/10.1074/jbc.m103377200.

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Thornton, Casey, Nichole Owen, Elizabeth Mizerik, et al. "P701: Novel presentation of dextrocardia in TGIF1-related holoprosencephaly." Genetics in Medicine Open 2 (2024): 101605. http://dx.doi.org/10.1016/j.gimo.2024.101605.

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Yan, L., B. Womack, D. Wotton, et al. "Tgif1 Regulates Quiescence and Self-Renewal of Hematopoietic Stem Cells." Molecular and Cellular Biology 33, no. 24 (2013): 4824–33. http://dx.doi.org/10.1128/mcb.01076-13.

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