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_4 label "Selventa" provenance.
_3 value "The HBP1 transcriptional repressor and the p38 MAP kinase: unlikely partners in G1 regulation and tumor suppression Amy S. Yee, a, b, c, , , Eric K. Paulsona, c, Michael A. McDevittd, Kimberly Rieger-Christe, Ian Summerhayese, Stephen P. Berasia, b, Jiyoung Kima, f, Chun-Yin Huangc and Xiaowei Zhanga a Department of Biochemistry, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA b Program in Genetics, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA c Department of Radiation Oncology, Tufts-New England Medical Center, 75 Kneeland St., Boston, MA 02111, USA d Department of Medicine, Division of Hematology, Johns Hopkins University School of Medicine, 720 Rutland Ave., Ross Research Building, Room 1025, Baltimore, MD 21205, USA e Cell and Molecular Biology Laboratory, R.E. Wise M.D. Research and Education Institute, Lahey Clinic, 31 Mall Road, Burlington, MA 01805, USA f Program in Cell and Molecular Nutrition, School of Nutrition Science and Policy, 150 Harrison Ave., Tufts University, Boston, MA 02111, USA Received 17 November 2003; Revised 3 March 2004; accepted 5 April 2004 Received by A.J. van Wijnen Available online 8 June 2004. Abstract Mechanisms that inhibit cell cycle progression and establish growth arrest are fundamental to tumor suppression and to normal cell differentiation. A complete understanding of these mechanisms should provide new diagnostic and therapeutic targets for future clinical applications related to cancer-specific pathways. This review will focus on the HMG-box protein 1 (HBP1) transcriptional repressor and its roles in cell cycle progression and tumor suppression. The work of several labs now suggests a new pathway for inhibiting G1 progression with exciting possible implications for tumor suppression. Our recent work suggests that the two previously unassociated proteins - the HBP1 transcription factor and the p38 MAP kinase pathway may now participate together in a G1 regulatory network. Several recent papers collectively highlight an unexpected role and connection of the p38 MAP kinase-signaling pathway in cell cycle control, senescence, and tumor suppression. Together, these initially divergent observations may provide clues into a new tumor suppressive network and spur further investigations that may contribute to new diagnostic and therapeutic targets for cancer. Author Keywords: HBP1; Tumor suppressor; p38 MAPK; Wnt signaling; AXH; Ataxin homology domain; HDAC; ROS; p47 phox; Chromosome 7 AML, acute myelogenous leukemia; APC, adenematous polypoisis coli; AXH, ataxin; GSK3b, glycogen synthase beta; HBP1, HMG box protein 1; HDAC, histone deacetylase; HMG, high mobility group; JNK, Jun activating kinase; LEF, lymphocyte enhancing factor; MAPK, mitogenactivated kinase; MKK3, MAP kinase kinase 3; MKK6, MAP kinase kinase 9; P38MAPK, p38 MAP kinase; RB, retinoblastoma; ROS, reactive oxygen species; TCF, T-cell factor Article Outline 1. Background 1.1. The RB/E2F paradigm and lessons for studying G1 regulation 1.1.1. Objective 2. The HBP1 transcription factor: pathways and gene targets 2.1. HBP1, G1 control and cancer 2.2. HBP1 transcription factor functions 2.2.1. DNA binding domain and specificity 2.2.2. Repression domain 2.3. Gene targets 2.3.1. Wnt target genes (Cyclin D1 and c-MYC) 2.3.1.1. Wnt signaling and cancer 2.3.1.2. Significance of HBP1 in Wnt signaling 2.3.2. p47 phox, reactive oxygen species, and growth factor signaling 2.3.2.1. Cell cycle and cancer implications 2.3.2.2. HBP1 and the p47 phox gene 2.3.3. Other genes 2.3.3.1. N-MYC 2.3.3.2. Histone H10 2.3.3.3. Locus control region and position-effect variegation 2.3.3.4. Myeloperoxidase 2.3.3.5. Summary 3. A new pathway for G1 regulation, senescence, and tumor suppression? 3.1. The basics of the p38 MAPK pathway 3.2. The roles of p38 MAPK, HBP1, p21 in G1 regulation 3.3. The p38 MAPK in senescence and tumor suppress..." provenance.
_3 wasQuotedFrom 15225871 provenance.
assertion hadPrimarySource 15225871 provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
assertion wasDerivedFrom _3 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
large_corpus.bel authoredBy _4 provenance.
large_corpus.bel version "20131211" provenance.