17 results on '"Matli, M"'
Search Results
2. Rheb activates AMPK and reduces p27Kip1 levels in Tsc2-null cells via mTORC1-independent mechanisms: implications for cell proliferation and tumorigenesis
- Author
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Lacher, M D, Pincheira, R, Zhu, Z, Camoretti-Mercado, B, Matli, M, Warren, R S, and Castro, A F
- Published
- 2010
- Full Text
- View/download PDF
3. Coordinated induction of VEGF receptors in mesenchymal cell types during rat hepatic wound healing
- Author
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Ankoma-Sey, V, Matli, M, Chang, K B, Lalazar, A, Donner, D B, Wong, L, Warren, R S, and Friedman, S L
- Published
- 1998
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4. Aspirations and needs of farmers on communal grazing areas in the Free State
- Author
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Masiteng, TJ, Van der Westhuizen, C, and Matli, M
- Abstract
The study evaluated the needs and aspirations of farmers in communal or commonage grazing systems in the Free State. The study focused on communal grazing systems in Qwaqwa, Thaba-Nchu, Botshabelo as well as parts of areas in the Free State where commonage grazing systems are practiced by small-scale farmers. In this study the needs and aspirations of the farmers are related to the integration of environmental planning into communal grazing systems in the Free State, as well as security of tenure, working capital, knowledge, adequate extension services, training and water supply, timely veld fires, and co-operation amongst farmers. The needs and aspirations of livestock owners in the communal rangelands of the Free State are constrained by small farm size, population pressure, land tenure problems, distance from markets, poor transport and infrastructure. The study also reveals that integration of environmental planning into communal grazing systems in the Free State is essential for the best cattle performance and land use. South African Journal of Agricultural Extension Vol.32 2003: 85-97
- Published
- 2004
5. Incomplete inhibition of phosphorylation of 4E-BP1 as a mechanism of primary resistance to ATP-competitive mTOR inhibitors
- Author
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Ducker, G S, primary, Atreya, C E, additional, Simko, J P, additional, Hom, Y K, additional, Matli, M R, additional, Benes, C H, additional, Hann, B, additional, Nakakura, E K, additional, Bergsland, E K, additional, Donner, D B, additional, Settleman, J, additional, Shokat, K M, additional, and Warren, R S, additional
- Published
- 2013
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6. Regulation by vascular endothelial growth factor of human colon cancer tumorigenesis in a mouse model of experimental liver metastasis.
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Warren, R S, primary, Yuan, H, additional, Matli, M R, additional, Gillett, N A, additional, and Ferrara, N, additional
- Published
- 1995
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7. Use of recombinant interferon to prevent recurrent herpesvirus shedding.
- Author
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Smolin, G., Matli, M., Okumoto, M., Mayers, M., and Samy, M.
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- 1984
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8. In vitro and in vivo Studies on Cefoperazone.
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Okumoto, M., Smolin, G., Grabner, G., Matli, M., Fuerst, D., and Zhang, W.
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- 1983
- Full Text
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9. Induction of vascular endothelial growth factor by insulin-like growth factor 1 in colorectal carcinoma.
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Warren, R S, Yuan, H, Matli, M R, Ferrara, N, and Donner, D B
- Abstract
Vascular endothelial growth factor (VEGF) is an angiogenic hormone that is produced by and supports the growth of many types of malignancies. The present study shows that insulin-like growth factor 1 (IGF-I), a mitogen that promotes the propagation of cancers through autocrine and paracrine mechanisms, increases the expression of mRNA for VEGF and production of VEGF protein by COLO 205 colon carcinoma cells. IGF-I also induces expression of VEGF mRNA in SW620, LSLiM6, and HCT15 colon carcinoma cells showing that this is a common response to IGF-I. Whereas IGF-I induced VEGF mRNA in each cell line examined (2.3-12-fold), it induced proliferation only in COLO 205 and LSLiM6 cells. Thus, the proliferative response induced by IGF-I and its ability to induce VEGF occur through distinguishable mechanisms. IGF-I increases the cellular content of VEGF mRNA by increasing the rate of transcription (5-fold after 4 h) and also by increasing the half-life of VEGF mRNA (0.6 +/- 0.07 h in control cells to 2.0 +/- 0.37 h in IGF-I-treated cells). Monoclonal antibody (alphaIR3) directed against the type 1 IGF receptor significantly attenuated the ability of IGF-I to promote expression of VEGF mRNA. Interestingly, by itself alphaIR3 acted as a weak agonist and induced a modest increase in the cellular content of VEGF mRNA. alphaIR3 also promoted tyrosine phosphorylation of the beta subunit of the IGF-I receptor, and the magnitude of this response was comparable with that induced by IGF-I. These observations point to a nonlinear relationship between activation of the IGF-I receptor and induction of VEGF mRNA. Thus, in addition to its direct, growth stimulatory effect on transformed cells, IGF-I induces the expression of VEGF which can promote the progression of cancer by regulating the development of new blood vessels.
- Published
- 1996
10. STAT3 regulates inflammatory cytokine production downstream of TNFR1 by inducing expression of TNFAIP3/A20.
- Author
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Antonia RJ, Karelehto E, Toriguchi K, Matli M, Warren RS, Pfeffer LM, and Donner DB
- Subjects
- Animals, Gene Expression, Inflammation, Janus Kinase 2 metabolism, Mice, Mice, Knockout, NF-kappa B metabolism, STAT3 Transcription Factor metabolism, Tumor Necrosis Factor alpha-Induced Protein 3 genetics, Tumor Necrosis Factor alpha-Induced Protein 3 metabolism, Receptors, Tumor Necrosis Factor, Type I genetics, Tumor Necrosis Factor-alpha metabolism
- Abstract
Tumour Necrosis Factor (TNF) potently induces a transient inflammatory response that must be downregulated once any invasive stimulus has resolved. Yet, how TNF-induced inflammation is shut down in normal cells is incompletely understood. The present study shows that STAT3 was activated in mouse embryo fibroblasts (MEFs) by treatment with TNF or an agonist antibody to TNFR1. STAT3 activation was inhibited by pharmacological inhibition of the Jak2 tyrosine kinase that associates with TNFR1. To identify STAT3 target genes, global transcriptome analysis by RNA sequencing was performed in wild-type MEFs and MEFs from STAT3 knockout (STAT3
KO ) mice that were stimulated with TNF, and the results were validated at the protein level by using multiplex cytokine assays and immunoblotting. After TNF stimulation, STAT3KO MEFs showed greater gene and protein induction of the inflammatory chemokines Ccl2, Cxcl1 and Cxcl10 than WT MEFs. These observations show that, by activating STAT3, TNF selectively modulates expression of a cohort of chemokines that promote inflammation. The greater induction by TNF of chemokines in STAT3KO than WT MEFs suggested that TNF induced an inhibitory protein in WT MEFs. Consistent with this possibility, STAT3 activation by TNFR1 increased the expression of Tnfaip3/A20, a ubiquitin modifying enzyme that inhibits inflammation, in WT MEFs but not in STAT3KO MEFs. Moreover, enforced expression of Tnfaip3/A20 in STAT3KO MEFs suppressed proinflammatory chemokine expression induced by TNF. Our observations identify Tnfaip3/A20 as a new downstream target for STAT3 which limits the induction of Ccl2, Cxcl1 and Cxcl10 and inflammation induced by TNF., (© 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)- Published
- 2022
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11. RasGRP1 is a potential biomarker to stratify anti-EGFR therapy response in colorectal cancer.
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Gbenedio OM, Bonnans C, Grun D, Wang CY, Hatch AJ, Mahoney MR, Barras D, Matli M, Miao Y, Garcia KC, Tejpar S, Delorenzi M, Venook AP, Nixon AB, Warren RS, Roose JP, and Depeille P
- Subjects
- Animals, Antineoplastic Agents, Immunological pharmacology, Biomarkers, Tumor analysis, Biomarkers, Tumor genetics, Cell Proliferation drug effects, Cetuximab pharmacology, Cetuximab therapeutic use, Clinical Trials as Topic, Colorectal Neoplasms mortality, Colorectal Neoplasms pathology, Computational Biology, DNA-Binding Proteins analysis, DNA-Binding Proteins genetics, Datasets as Topic, Disease Models, Animal, Disease Progression, Disease-Free Survival, ErbB Receptors antagonists & inhibitors, ErbB Receptors metabolism, Guanine Nucleotide Exchange Factors analysis, Guanine Nucleotide Exchange Factors genetics, Humans, Kaplan-Meier Estimate, Mice, Mice, Knockout, Primary Cell Culture, Prognosis, Signal Transduction drug effects, Spheroids, Cellular, Tumor Cells, Cultured, Tumor Suppressor Proteins analysis, Tumor Suppressor Proteins genetics, Antineoplastic Agents, Immunological therapeutic use, Biomarkers, Tumor metabolism, Colorectal Neoplasms drug therapy, DNA-Binding Proteins metabolism, Guanine Nucleotide Exchange Factors metabolism, Tumor Suppressor Proteins metabolism
- Abstract
Colorectal cancer (CRC) is the third most frequent neoplastic disorder and is a main cause of tumor-related mortality as many patients progress to stage IV metastatic CRC. Standard care consists of combination chemotherapy (FOLFIRI or FOLFOX). Patients with WT KRAS typing are eligible to receive anti-EGFR therapy combined with chemotherapy. Unfortunately, predicting efficacy of CRC anti-EGFR therapy has remained challenging. Here we uncover that the EGFR-pathway component RasGRP1 acts as CRC tumor suppressor in the context of aberrant Wnt signaling. We find that RasGRP1 suppresses EGF-driven proliferation of colonic epithelial organoids. Having established that RasGRP1 dosage levels impacts biology, we focused on CRC patients next. Mining five different data platforms, we establish that RasGRP1 expression levels decrease with CRC progression and predict poor clinical outcome of patients. Lastly, deletion of one or two Rasgrp1 alleles makes CRC spheroids more susceptible to EGFR inhibition. Retrospective analysis of the CALGB80203 clinical trial shows that addition of anti-EGFR therapy to chemotherapy significantly improves outcome for CRC patients when tumors express low RasGRP1 suppressor levels. In sum, RasGRP1 is a unique biomarker positioned in the EGFR pathway and of potential relevance to anti-EGFR therapy for CRC patients.
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- 2019
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12. RasGRP1 opposes proliferative EGFR-SOS1-Ras signals and restricts intestinal epithelial cell growth.
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Depeille P, Henricks LM, van de Ven RA, Lemmens E, Wang CY, Matli M, Werb Z, Haigis KM, Donner D, Warren R, and Roose JP
- Subjects
- Adenomatous Polyposis Coli Protein genetics, Animals, Cell Differentiation genetics, Cell Line, Tumor, Cell Proliferation, Colorectal Neoplasms metabolism, Epithelial Cells metabolism, Guanine Nucleotide Exchange Factors biosynthesis, Humans, Intestinal Mucosa cytology, Mice, Mice, Inbred C57BL, Mice, Knockout, Neoplasm Transplantation, Proto-Oncogene Proteins p21(ras) genetics, RNA Interference, RNA, Small Interfering, Signal Transduction, Transplantation, Heterologous, Wnt Proteins genetics, Wnt Signaling Pathway genetics, ErbB Receptors metabolism, Guanine Nucleotide Exchange Factors genetics, Intestinal Mucosa metabolism, SOS1 Protein metabolism
- Abstract
The character of EGFR signals can influence cell fate but mechanistic insights into intestinal EGFR-Ras signalling are limited. Here we show that two distinct Ras nucleotide exchange factors, RasGRP1 and SOS1, lie downstream of EGFR but act in functional opposition. RasGRP1 is expressed in intestinal crypts where it restricts epithelial growth. High RasGRP1 expression in colorectal cancer (CRC) patient samples correlates with a better clinical outcome. Biochemically, we find that RasGRP1 creates a negative feedback loop that limits proliferative EGFR-SOS1-Ras signals in CRC cells. Genetic Rasgrp1 depletion from mice with either an activating mutation in KRas or with aberrant Wnt signalling due to a mutation in Apc resulted in both cases in exacerbated Ras-ERK signalling and cell proliferation. The unexpected opposing cell biological effects of EGFR-RasGRP1 and EGFR-SOS1 signals in the same cell shed light on the intricacy of EGFR-Ras signalling in normal epithelium and carcinoma.
- Published
- 2015
- Full Text
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13. Hypoxia-induced radioresistance is independent of hypoxia-inducible factor-1A in vitro.
- Author
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Arvold ND, Guha N, Wang D, Matli M, Deen DF, Warren RS, and Haas-Kogan DA
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- Animals, Cell Line, Transformed metabolism, Cell Line, Transformed radiation effects, Fibroblasts metabolism, Fibroblasts radiation effects, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Cell Hypoxia physiology, Radiation Tolerance physiology, Transcription Factors metabolism
- Abstract
Purpose: We sought to determine whether hypoxia-induced radioresistance is mediated by the transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha)., Methods and Materials: We used 2 mouse embryonic fibroblast cell lines transformed with H-ras and TAg, 1 HIF-1alpha+/+ and the other HIF-1alpha-/-. Cell were exposed to either 95% air and 5% CO2 (normoxic conditions) or 0.2% O2, 94.8% N2, and 5% CO2 (hypoxic conditions) for 4 hours. Cells were then irradiated and subjected to clonogenic survival assays., Results: Whereas neither +/+ ras/TAg nor -/- ras/TAg cells expressed HIF-1alpha under normoxic conditions, hypoxia induced expression of HIF-1alpha only in +/+ ras/TAg cells, confirming the absence of HIF-1alpha in -/- ras/TAg cells. Clonogenic survival curves for +/+ ras/TAg and -/- ras/TAg cells under normoxia and hypoxia demonstrated that hypoxia increased radioresistance in both cell lines to the same degree. At 1-log cell kill, the +/+ ras/TAg and -/- ras/TAg cells had an identical oxygen enhancement ratio of 1.28 +/- 0.09 and nearly identical oxygen enhancement ratios at 2-log cell kill., Conclusion: In our system of transformed mouse embryonic fibroblasts, hypoxia-mediated radiation resistance is independent of HIF-1alpha.
- Published
- 2005
- Full Text
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14. Recombinant IL-4 inhibits IL-6 synthesis by adherent peripheral blood cells in vitro.
- Author
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Gibbons R, Martinez O, Matli M, Heinzel F, Bernstein M, and Warren R
- Subjects
- Acute-Phase Reaction immunology, Cell Adhesion, Humans, In Vitro Techniques, Interleukin-6 blood, Kinetics, Leukocytes, Mononuclear cytology, Leukocytes, Mononuclear metabolism, Lipopolysaccharides pharmacology, RNA, Messenger biosynthesis, Recombinant Proteins pharmacology, Tetradecanoylphorbol Acetate, Interleukin-4 pharmacology, Interleukin-6 biosynthesis, Leukocytes, Mononuclear drug effects
- Abstract
IL-4 has been shown to participate in interregulatory networks with other cytokines including IL-2, IFN-gamma, IL-1 beta, and TNF-alpha. The ability of recombinant IL-4 (rIL-4) to modulate the synthesis and release of IL-6 was investigated in vitro. LPS-stimulated adherent cells (AC) from human peripheral blood secreted IL-6 as determined by ELISA and bioassay with the B9 hybridoma cell line. The secretion of IL-6 peaked between 12-16 h after LPS stimulation. The addition of rIL-4 inhibited LPS-induced IL-6 production measured at 8 h. The inhibitory effect of rIL-4 on IL-6 secretion was dose-dependent and occurred at doses as low as 0.001 U/ml (0.01 pg/ml). Recombinant IL-4 was added to the cultures for various periods and removed by aspiration of the medium and washing the cells. The subsequent LPS-induction of IL-6 secretion was reduced in cultures exposed to rIL-4 for as little as 5 minutes indicating that the effect of rIL-4 on the monocytes was rapid and irreversible. Northern blot analysis revealed that the effect of rIL4 on LPS-induced production of IL-6 by AC occurred at least in part at the level of transcription. In contrast, PMA-induced IL-6 gene transcription was not affected by rIL-4. These findings indicate that rIL-4 can regulate the synthesis of IL-6 by adherent peripheral blood mononuclear cells.
- Published
- 1990
15. Recombinant human interferon alpha D in HSV-1 recurrence in the rabbit.
- Author
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Mayers M, Matli M, Okumoto M, Samy M, and Smolin G
- Subjects
- Animals, DNA, Recombinant, Drug Administration Schedule, Epinephrine therapeutic use, Hydroxydopamines pharmacology, Interferon Type I administration & dosage, Interferon Type I metabolism, Iontophoresis, Keratitis, Dendritic metabolism, Keratitis, Dendritic prevention & control, Ophthalmic Solutions, Oxidopamine, Rabbits, Recurrence, Sodium Chloride therapeutic use, Tears metabolism, Interferon Type I therapeutic use, Keratitis, Dendritic drug therapy
- Abstract
Recombinant human interferon alpha subtype D (RIFN alpha D) was effective in reducing the shedding of herpes simplex virus type-1 (HSV-1) induced by 6-hydroxydopamine iontophoresis followed by topical epinephrine application in previously infected rabbit corneas. A treatment schedule of RIFN alpha D, two drops QID was superior to one drop BID. RIFN alpha A also appeared to be effective in reducing viral shedding. Rabbits treated with RIFN alpha D during two episodes of adrenergically induced HSV-1 shedding, but not during anticipated episodes of spontaneous shedding, did not show a significant reduction in shedding of virus. Interferon was present in significantly higher concentration in tear samples following treatment with RIFN alpha D as compared with RIFN alpha A.
- Published
- 1985
16. Interferon effects on herpes simplex virus in rabbit and human cell cultures.
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Fuerst DJ, Matli M, Smolin G, and O'Donnell J
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- Animals, Cells, Cultured, Cornea cytology, Humans, Interferon Type I classification, Kidney cytology, Osmolar Concentration, Rabbits, Recombinant Proteins, Viral Plaque Assay, Interferon Type I pharmacology, Simplexvirus drug effects
- Abstract
The effects of four subtypes of recombinant human alpha interferon (RIFN alpha), (A,B,D, and the hybrid A/D) were tested on six strains of herpes simplex virus (HSV). RIFN alpha -D was the most effective subtype in rabbit kidney cells, which is consistent with our previous in vivo results in the rabbit herpetic keratitis model. In human corneal cells, however, RIFN alpha -D was one of the least effective IFN subtypes tested. Conversely, RIFN alpha-A appeared to be relatively more effective in the human corneal cells than in the rabbit kidney cells, but RIFN alpha -B and RIFN alpha -A/D were the most effective interferon subtypes in human corneal cells. Different strains of HSV had different susceptibilities to the various IFN subtypes tested.
- Published
- 1986
- Full Text
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17. Use of recombinant interferon in HSV-1 recurrence in the rabbit.
- Author
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Matli M, Smolin G, and Okumoto M
- Subjects
- Animals, Cell Count, Cell Line, Cornea pathology, Interferons metabolism, Keratitis, Dendritic microbiology, Male, Rabbits, Recombinant Proteins metabolism, Recurrence, Simplexvirus isolation & purification, Tears metabolism, Tears microbiology, Interferons therapeutic use, Keratitis, Dendritic drug therapy, Recombinant Proteins therapeutic use
- Abstract
The use of recombinant human interferon alpha subtype D (RIFN alpha D) was effective in reducing shedding of herpes simplex virus type-1 induced by iontophoresis of 6-hydroxydopamine and epinephrine. A post stimulation treatment schedule of RIFN alpha D, one drop four times a day was as effective as pretreatment, using the same dose regimen. The levels of interferon (IFN) present in the assay system are not sufficient to produce an antiviral effect. The levels of IFN required to suppress cell growth are substantially higher than the concentrations detected in the assay system.
- Published
- 1987
- Full Text
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