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1

Nuchprayoon, I., S. Meyers, L. M. Scott, J. Suzow, S. Hiebert, and A. D. Friedman. "PEBP2/CBF, the murine homolog of the human myeloid AML1 and PEBP2 beta/CBF beta proto-oncoproteins, regulates the murine myeloperoxidase and neutrophil elastase genes in immature myeloid cells." Molecular and Cellular Biology 14, no. 8 (1994): 5558–68. http://dx.doi.org/10.1128/mcb.14.8.5558.

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The myeloperoxidase (MPO) and neutrophil elastase genes are expressed specifically in immature myeloid cells. The integrity of a polyomavirus enhancer core sequence, 5'-AACCACA-3', is critical to the activity of the murine MPO proximal enhancer. This element binds two species, myeloid nuclear factors 1 alpha and 1 beta (MyNF1 alpha and -beta), present in 32D cl3 myeloid cell nuclear extracts. The levels of the MyNF1s increase during early 32D cl3 cell granulocytic differentiation. Both MyNF1 alpha and -beta supershift with an antiserum raised by using a peptide derived from the N terminus of p
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2

Nuchprayoon, I., S. Meyers, L. M. Scott, J. Suzow, S. Hiebert, and A. D. Friedman. "PEBP2/CBF, the murine homolog of the human myeloid AML1 and PEBP2 beta/CBF beta proto-oncoproteins, regulates the murine myeloperoxidase and neutrophil elastase genes in immature myeloid cells." Molecular and Cellular Biology 14, no. 8 (1994): 5558–68. http://dx.doi.org/10.1128/mcb.14.8.5558-5568.1994.

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The myeloperoxidase (MPO) and neutrophil elastase genes are expressed specifically in immature myeloid cells. The integrity of a polyomavirus enhancer core sequence, 5'-AACCACA-3', is critical to the activity of the murine MPO proximal enhancer. This element binds two species, myeloid nuclear factors 1 alpha and 1 beta (MyNF1 alpha and -beta), present in 32D cl3 myeloid cell nuclear extracts. The levels of the MyNF1s increase during early 32D cl3 cell granulocytic differentiation. Both MyNF1 alpha and -beta supershift with an antiserum raised by using a peptide derived from the N terminus of p
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3

Steensma, David P., Richard J. Gibbons, Ruben A. Mesa, Ayalew Tefferi, and Douglas R. Higgs. "Somatic Point Mutations in RUNX1/CBFA2/AML1 Are Common in High-Risk Myelodysplastic Syndrome, but Not in Myelofibrosis with Myeloid Metaplasia." Blood 104, no. 11 (2004): 2438. http://dx.doi.org/10.1182/blood.v104.11.2438.2438.

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Abstract Introduction: The core-binding factor subunit RUNX1/CBFA2/AML1 (Runt-related transcription factor 1, Core-binding factor alpha 2 subunit, Oncogene AML1) is critical for generation of hematopoietic stem cells during embryogenesis and for normal megakaryopoiesis in adults. RUNX1/CBFA2/AML1 has long been recognized as an oncogene, and is frequently involved in leukemia-associated translocations that create aberrant fusion proteins (e.g., AML1-ETO). Recently, acquired somatic point mutations in the RUNX1/CBFA2/AML1 gene have been described in a subset of patients with myelodysplastic synd
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4

Hamey, Fiona K., Sonia Nestorowa, Sarah J. Kinston, David G. Kent, Nicola K. Wilson, and Berthold Göttgens. "Reconstructing blood stem cell regulatory network models from single-cell molecular profiles." Proceedings of the National Academy of Sciences 114, no. 23 (2017): 5822–29. http://dx.doi.org/10.1073/pnas.1610609114.

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Adult blood contains a mixture of mature cell types, each with specialized functions. Single hematopoietic stem cells (HSCs) have been functionally shown to generate all mature cell types for the lifetime of the organism. Differentiation of HSCs toward alternative lineages must be balanced at the population level by the fate decisions made by individual cells. Transcription factors play a key role in regulating these decisions and operate within organized regulatory programs that can be modeled as transcriptional regulatory networks. As dysregulation of single HSC fate decisions is linked to f
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5

Qi, Xiangjun, Hongbin Xu, Peng Zhang, et al. "Investigating the Mechanism of Scutellariae barbata Herba in the Treatment of Colorectal Cancer by Network Pharmacology and Molecular Docking." Evidence-Based Complementary and Alternative Medicine 2021 (August 2, 2021): 1–18. http://dx.doi.org/10.1155/2021/3905367.

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Background. Colorectal cancer (CRC) is one of the most common gastrointestinal tumors, which accounts for approximately 10% of all diagnosed cancers and cancer deaths worldwide per year. Scutellariae barbatae Herba (SBH) is one of the most frequently used traditional Chinese medicine (TCM) in the treatment of CRC. Although many experiments have been carried out to explain the mechanisms of SBH, the mechanisms of SBH have not been illuminated fully. Thus, we constructed a network pharmacology and molecular docking to investigate the mechanisms of SBH. Methods. We adopted active constituent pres
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6

Cammenga, Jorg, Gabriela Putz, Birte Niebuhr, et al. "The Role of RUNX1 DNA-Binding Mutations in Acute Myeloid Leukemia." Blood 106, no. 11 (2005): 1373. http://dx.doi.org/10.1182/blood.v106.11.1373.1373.

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Abstract The RUNX1 gene encodes an alpha subunit of the core-binding factor (CBF), an important heterodimeric transcription factor in hematopoietic ontogeny and development, and is one of the most frequently disrupted genes in acute leukemia. In addition to its involvement in several translocations, the RUNX1 gene is often subject to deletions or point mutations in acute myelogenous leukemia (AML). Interestingly, in addition to complete loss-of-function mutations, many of the alterations involve missense point mutations within the Runt domain that disrupt DNA binding activity (DB-mutants). In
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7

Fang, Yue, Xinquan Liu, and Jing Su. "Network Pharmacology Analysis of Traditional Chinese Medicine Formula Shuang Di Shou Zhen Tablets Treating Nonexudative Age-Related Macular Degeneration." Evidence-Based Complementary and Alternative Medicine 2021 (March 24, 2021): 1–14. http://dx.doi.org/10.1155/2021/6657521.

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Objective. To analyze the pharmacological mechanism of the treatment of dry age-related macular degeneration (dry AMD) based on a network pharmacological approach of Shuang Di Shou Zhen Tablets (SDSZT) and to provide a new reference for the current lack of effective treatment of dry AMD. Methods. The main chemical constituents and their targets of Rehmanniae Radix Praeparata, Ligustrum lucidum, Mori Fructus, Paeonia albiflora, Rhizoma Dioscoreae, Alisma orientale, Schisandra chinensis, Radix Polygoni Multiflori Preparata, Ophiopogon japonicus, and Radix Rehmanniae were obtained from the Tradit
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8

Burda, Pavel, Nikola Curik, Juraj Kokavec, et al. "PU.1 Relieves Its GATA-1-Mediated Repression near Cebpa and Cbfb During Transdifferentiation of Murine Erythroleukemia - Tool of Inducing Leukemic Blasts to Differentiate." Blood 114, no. 22 (2009): 547. http://dx.doi.org/10.1182/blood.v114.22.547.547.

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Abstract Abstract 547 Transcription factors GATA-1 and PU.1 interact on DNA to block transcriptional programs of undesired lineage during hematopoietic commitment. Murine erythroleukemia (MEL) cells that co-express GATA-1 and PU.1 are blocked at the blast stage but respond to down-regulation of PU.1 or up-regulation of GATA-1 by inducing terminal erythroid differentiation. To test whether GATA-1 blocks PU.1 in MEL cells we have conditionally activated a transgenic PU.1 protein fused with the estrogen receptor ligand-binding domain (PUER), resulting in activation of a myeloid transcriptional pr
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9

Stopka, Tomas, Pavel Burda, Petra Basova, et al. "5-Azacytidine and G-CSF Derepressed Chromatin Structure of PU.1 and Its Targets Cebpa and Cbfb In Myelodysplastic Syndrome (MDS)." Blood 116, no. 21 (2010): 124. http://dx.doi.org/10.1182/blood.v116.21.124.124.

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Abstract Abstract 124 The myelodysplastic syndrome (MDS) represents a heterogeneous disorder characterized by ineffective hematopoiesis and evolution to acute myelogenous leukemia that is strikingly refractory to current therapeutic approaches. Novel epigenetic drugs including DNA-methyltransferase inhibitor 5-Azacitidine (5-AZA, Vidaza) are currently considered to improve clinical response in patients with MDS. MDS is characterized by abnormal differentiation and blocked maturation responsive to 5-AZA, therefore we studied major regulator of hematopoietic differentiation, transcription factor
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10

Kutny, Matthew A., Todd A. Alonzo, Robert B. Gerbing, et al. "RUNX1 Mutations in Pediatric AML: A Report From the Children's Oncology Group." Blood 114, no. 22 (2009): 2614. http://dx.doi.org/10.1182/blood.v114.22.2614.2614.

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Abstract Abstract 2614 Poster Board II-590 The RUNX1 gene (previously AML1) encodes the alpha subunit of core binding factor (CBFα), which is implicated in normal and malignant hematopoiesis. Translocations involving RUNX1 have been associated with favorable prognosis in acute leukemias (e.g., t(8;21) in AML and t(12;21) in ALL). Point mutations of RUNX1 have been identified in exon 3 and exon 8 of the RUNX1 gene in a subset of AML patients and are most closely associated with MDS associated AML and AML subtype M0. We evaluated the prevalence and prognostic significance of RUNX1 mutations in p
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11

Scott, C. D., and R. C. Baxter. "Synthesis of the acid-labile subunit of the growth-hormone-dependent insulin-like-growth-factor-binding protein complex by rat hepatocytes in culture." Biochemical Journal 275, no. 2 (1991): 441–46. http://dx.doi.org/10.1042/bj2750441.

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Insulin-like growth factors (IGFs) circulate predominantly in a growth-hormone-dependent ternary complex of 125-150 kDa. This study investigates the production of the alpha-subunit of this complex, an acid-labile glycoprotein without intrinsic IGF-binding activity, which binds to the IGF-binding protein IGFBP-3 in the presence of IGFs. Medium conditioned by primary cultures of rat hepatocytes produced alpha-subunit with similar complex-forming activity to purified rat serum alpha-subunit. Bovine growth hormone stimulated hepatocyte production of both IGF-I and alpha-subunit. IGF-I tracer bound
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12

Baxter, R. C. "Glycosaminoglycans inhibit formation of the 140 kDa insulin-like growth factor-binding protein complex." Biochemical Journal 271, no. 3 (1990): 773–77. http://dx.doi.org/10.1042/bj2710773.

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The 140 kDa insulin-like growth factor (IGF)-binding protein complex in human serum consists of three subunits: an acid-labile, non-IGF-binding glycoprotein (alpha-subunit), an IGF-binding glycoprotein known as BP-53 or IGFBP-3 (beta-subunit), and IGF-I or IGF-II (gamma-subunit). This study investigates the regulation, by salt and glycosaminoglycans, of ternary (alpha-beta-gamma) complex formation, measured by incubating radioiodinated alpha-subunit with a mixture of IGF-I and IGFBP-3 and precipitating bound radioactivity with an anti-IGFBP-3 antiserum. Increasing NaCl concentrations progressi
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13

Park, Kyung-Ran, Joon-Yeop Lee, Myounglae Cho, Jin-Tae Hong, and Hyung-Mun Yun. "Paeonolide as a Novel Regulator of Core-Binding Factor Subunit Alpha-1 in Bone-Forming Cells." International Journal of Molecular Sciences 22, no. 9 (2021): 4924. http://dx.doi.org/10.3390/ijms22094924.

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Paeonia suffruticosa has been extensively used as a traditional medicine with various beneficial effects; paeonolide (PALI) was isolated from its dried roots. This study aimed to investigate the novel effects and mechanisms of PALI in pre-osteoblasts. Here, cell viability was evaluated using an MTT assay. Early and late osteoblast differentiation was examined by analyzing the activity of alkaline phosphatase (ALP) and by staining it with Alizarin red S (ARS). Cell migration was assessed using wound healing and Boyden chamber assays. Western blot and immunofluorescence analyses were used to exa
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14

Beghini, Alessandro. "Core Binding Factor Leukemia: Chromatin Remodeling Moves Towards Oncogenic Transcription." Cancers 11, no. 12 (2019): 1973. http://dx.doi.org/10.3390/cancers11121973.

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Acute myeloid leukemia (AML), the most common acute leukemia in adults, is a heterogeneous malignant clonal disorder arising from multipotent hematopoietic progenitor cells characterized by genetic and concerted epigenetic aberrations. Core binding factor-Leukemia (CBFL) is characterized by the recurrent reciprocal translocations t(8;21)(q22;q22) or inv(16)(p13;q22) that, expressing the distinctive RUNX1-RUNX1T1 (also known as Acute myeloid leukemia1-eight twenty-one, AML1-ETO or RUNX1/ETO) or CBFB-MYH11 (also known as CBFβ-SMMHC) translocation product respectively, disrupt the essential hemat
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15

McGlade, C. J., C. Ellis, M. Reedijk, et al. "SH2 domains of the p85 alpha subunit of phosphatidylinositol 3-kinase regulate binding to growth factor receptors." Molecular and Cellular Biology 12, no. 3 (1992): 991–97. http://dx.doi.org/10.1128/mcb.12.3.991.

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The binding of cytoplasmic signaling proteins such as phospholipase C-gamma 1 and Ras GTPase-activating protein to autophosphorylated growth factor receptors is directed by their noncatalytic Src homology region 2 (SH2) domains. The p85 alpha regulatory subunit of phosphatidylinositol (PI) 3-kinase, which associates with several receptor protein-tyrosine kinases, also contains two SH2 domains. Both p85 alpha SH2 domains, when expressed individually as fusion proteins in bacteria, bound stably to the activated beta receptor for platelet-derived growth factor (PDGF). Complex formation required P
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16

McGlade, C. J., C. Ellis, M. Reedijk, et al. "SH2 domains of the p85 alpha subunit of phosphatidylinositol 3-kinase regulate binding to growth factor receptors." Molecular and Cellular Biology 12, no. 3 (1992): 991–97. http://dx.doi.org/10.1128/mcb.12.3.991-997.1992.

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The binding of cytoplasmic signaling proteins such as phospholipase C-gamma 1 and Ras GTPase-activating protein to autophosphorylated growth factor receptors is directed by their noncatalytic Src homology region 2 (SH2) domains. The p85 alpha regulatory subunit of phosphatidylinositol (PI) 3-kinase, which associates with several receptor protein-tyrosine kinases, also contains two SH2 domains. Both p85 alpha SH2 domains, when expressed individually as fusion proteins in bacteria, bound stably to the activated beta receptor for platelet-derived growth factor (PDGF). Complex formation required P
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17

Rapoport, AP, S. Luhowskyj, P. Doshi, and JF DiPersio. "Mutational analysis of the alpha subunit of the human interleukin-3 receptor." Blood 87, no. 1 (1996): 112–22. http://dx.doi.org/10.1182/blood.v87.1.112.112.

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Abstract The alpha subunit of the human interleukin-3 receptor (IL-3R alpha) is a 70-kD glycoprotein member of the hematopoietin receptor superfamily. This protein associates with a beta subunit common to the receptors for IL-5 and granulocyte-macrophage colony-stimulating factor (GM-CSF) to form a high-affinity receptor for IL-3. To identify regions of IL-3R alpha critical for ligand binding and receptor function, cDNAs encoding mutant receptors were generated and expressed in COS cells along with the beta subunit. Mutant receptors lacking almost the entire cytoplasmic domain of IL-3R alpha [
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18

Rapoport, AP, S. Luhowskyj, P. Doshi, and JF DiPersio. "Mutational analysis of the alpha subunit of the human interleukin-3 receptor." Blood 87, no. 1 (1996): 112–22. http://dx.doi.org/10.1182/blood.v87.1.112.bloodjournal871112.

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The alpha subunit of the human interleukin-3 receptor (IL-3R alpha) is a 70-kD glycoprotein member of the hematopoietin receptor superfamily. This protein associates with a beta subunit common to the receptors for IL-5 and granulocyte-macrophage colony-stimulating factor (GM-CSF) to form a high-affinity receptor for IL-3. To identify regions of IL-3R alpha critical for ligand binding and receptor function, cDNAs encoding mutant receptors were generated and expressed in COS cells along with the beta subunit. Mutant receptors lacking almost the entire cytoplasmic domain of IL-3R alpha [IL-3R alp
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19

Calvete, J. J., A. Henschen та J. González-Rodríguez. "Assignment of disulphide bonds in human platelet GPIIIa. A disulphide pattern for the β-subunits of the integrin family". Biochemical Journal 274, № 1 (1991): 63–71. http://dx.doi.org/10.1042/bj2740063.

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Integrins are cell-surface heterodimers formed by the association of one alpha- and one beta-subunit. Glycoprotein IIIa (GPIIIa or beta 3 subunit) is the common beta-subunit of the beta 3 subfamily of integrins, which, when associated with glycoprotein IIb (GPIIb), constitutes the receptor for fibrinogen and other adhesive proteins at the platelet surface (the GPIIb-IIIa complex) and, when associated with the alpha v-subunit, constitutes the vitronectin receptor present in several cell types. Protein chemical analysis of GPIIIa allows us to define the following structural domains: the cysteine
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20

Goldfeld, A. E., E. Tsai, R. Kincaid, et al. "Calcineurin mediates human tumor necrosis factor alpha gene induction in stimulated T and B cells." Journal of Experimental Medicine 180, no. 2 (1994): 763–68. http://dx.doi.org/10.1084/jem.180.2.763.

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The tumor necrosis factor alpha (TNF-alpha) gene is rapidly transcribed in activated T cells via a calcium-dependent pathway that does not require de novo protein synthesis, but is completely blocked by the immunosuppressive drugs cyclosporin A (CsA) and FK506. Here we show that calcineurin phosphatase activity is both necessary and sufficient for TNF-alpha gene transcription in T cells, and identify the factor that binds to the kappa 3 element of the TNF-alpha gene promoter as the target for calcineurin action. The ability of analogues of CsA and FK506 to block calcineurin phosphatase activit
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21

Lagna, G., R. Kovelman, J. Sukegawa, and R. G. Roeder. "Cloning and characterization of an evolutionarily divergent DNA-binding subunit of mammalian TFIIIC." Molecular and Cellular Biology 14, no. 5 (1994): 3053–64. http://dx.doi.org/10.1128/mcb.14.5.3053.

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Transcription factor IIIC (TFIIIC) is required for the assembly of a preinitiation complex on 5S RNA, tRNA, and adenovirus VA RNA genes and contains two separable components, TFIIIC1 and TFIIIC2. TFIIIC2 binds to the 3' end of the internal control region of the VAI RNA gene and contains five polypeptides ranging in size from 63 to 220 kDa; the largest of these directly contacts DNA. Here we describe the cloning of cDNAs encoding all (rat) or part (human) of the 220-kDa subunit (TFIIIC alpha). Surprisingly, TFIIIC alpha has no homology to any of the yeast TFIIIC subunits already cloned, suggest
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22

Lagna, G., R. Kovelman, J. Sukegawa, and R. G. Roeder. "Cloning and characterization of an evolutionarily divergent DNA-binding subunit of mammalian TFIIIC." Molecular and Cellular Biology 14, no. 5 (1994): 3053–64. http://dx.doi.org/10.1128/mcb.14.5.3053-3064.1994.

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Transcription factor IIIC (TFIIIC) is required for the assembly of a preinitiation complex on 5S RNA, tRNA, and adenovirus VA RNA genes and contains two separable components, TFIIIC1 and TFIIIC2. TFIIIC2 binds to the 3' end of the internal control region of the VAI RNA gene and contains five polypeptides ranging in size from 63 to 220 kDa; the largest of these directly contacts DNA. Here we describe the cloning of cDNAs encoding all (rat) or part (human) of the 220-kDa subunit (TFIIIC alpha). Surprisingly, TFIIIC alpha has no homology to any of the yeast TFIIIC subunits already cloned, suggest
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23

Hajra, A., P. P. Liu, N. A. Speck, and F. S. Collins. "Overexpression of core-binding factor alpha (CBF alpha) reverses cellular transformation by the CBF beta-smooth muscle myosin heavy chain chimeric oncoprotein." Molecular and Cellular Biology 15, no. 9 (1995): 4980–89. http://dx.doi.org/10.1128/mcb.15.9.4980.

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A fusion between the transcription factor core-binding factor beta (CBF beta; also known as PEBP2 beta) and the tail region of smooth muscle myosin heavy chain (SMMHC) is generated by an inversion of chromosome 16 [inv(16) (p13q22)] associated with the M4Eo subtype of acute myeloid leukemia. We have previously shown that this CBF beta-SMMHC chimeric protein can transform NIH 3T3 cells and that this process requires regions of the chimeric protein necessary for association with the CBF alpha subunit. In this study, we show that NIH 3T3 cells overexpressing murine Cbf alpha 2 (also known as Aml1
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24

Watanabe, Y., T. Kitamura, K. Hayashida, and A. Miyajima. "Monoclonal antibody against the common beta subunit (beta c) of the human interleukin-3 (IL-3), IL-5, and granulocyte-macrophage colony- stimulating factor receptors shows upregulation of beta c by IL-1 and tumor necrosis factor-alpha." Blood 80, no. 9 (1992): 2215–20. http://dx.doi.org/10.1182/blood.v80.9.2215.2215.

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Abstract High-affinity receptors for human granulocyte macrophage colony- stimulating factor (GM-CSF), interleukin-3 (IL-3), and IL-5 are composed of two distinct subunits, alpha and beta. Each receptor has its own ligand-specific alpha subunit, and the three receptors share the common beta subunit, beta c. Using a transfectant of NIH3T3 cells expressing the high-affinity human GM-CSF receptor, monoclonal antibodies (MoAbs) against beta c were generated. These MoAbs specifically bound to cells bearing beta c and immunoprecipitated the beta c protein of 120 Kd. Using these MoAbs, expression of
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25

Watanabe, Y., T. Kitamura, K. Hayashida, and A. Miyajima. "Monoclonal antibody against the common beta subunit (beta c) of the human interleukin-3 (IL-3), IL-5, and granulocyte-macrophage colony- stimulating factor receptors shows upregulation of beta c by IL-1 and tumor necrosis factor-alpha." Blood 80, no. 9 (1992): 2215–20. http://dx.doi.org/10.1182/blood.v80.9.2215.bloodjournal8092215.

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High-affinity receptors for human granulocyte macrophage colony- stimulating factor (GM-CSF), interleukin-3 (IL-3), and IL-5 are composed of two distinct subunits, alpha and beta. Each receptor has its own ligand-specific alpha subunit, and the three receptors share the common beta subunit, beta c. Using a transfectant of NIH3T3 cells expressing the high-affinity human GM-CSF receptor, monoclonal antibodies (MoAbs) against beta c were generated. These MoAbs specifically bound to cells bearing beta c and immunoprecipitated the beta c protein of 120 Kd. Using these MoAbs, expression of beta c wa
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26

Kitamura, T., and A. Miyajima. "Functional reconstitution of the human interleukin-3 receptor." Blood 80, no. 1 (1992): 84–90. http://dx.doi.org/10.1182/blood.v80.1.84.84.

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Abstract The high-affinity receptors for human interleukin-3 (IL-3), GM-CSF, and IL-5 are composed of alpha and beta subunits. The alpha subunits are primary ligand binding proteins specific for each ligand, whereas the three human receptors share a common beta subunit (beta c). In contrast to humans mice have two closely related genes, AIC2A and AIC2B, which are homologous to human beta c. The AIC2A gene encodes a low-affinity murine IL-3 binding protein, and the AIC2B protein is the beta subunit shared between murine GM-CSF receptors (mGMR) and IL-5 receptors (mIL- 5R). To examine the functi
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27

Kitamura, T., and A. Miyajima. "Functional reconstitution of the human interleukin-3 receptor." Blood 80, no. 1 (1992): 84–90. http://dx.doi.org/10.1182/blood.v80.1.84.bloodjournal80184.

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The high-affinity receptors for human interleukin-3 (IL-3), GM-CSF, and IL-5 are composed of alpha and beta subunits. The alpha subunits are primary ligand binding proteins specific for each ligand, whereas the three human receptors share a common beta subunit (beta c). In contrast to humans mice have two closely related genes, AIC2A and AIC2B, which are homologous to human beta c. The AIC2A gene encodes a low-affinity murine IL-3 binding protein, and the AIC2B protein is the beta subunit shared between murine GM-CSF receptors (mGMR) and IL-5 receptors (mIL- 5R). To examine the function of the
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28

Guo, Yalin, Laleh Talebian, Ivan Maillard та ін. "Reduction of Core Binding Factor beta (CBFβ) Dosage Blocks T Cell Development." Blood 106, № 11 (2005): 2714. http://dx.doi.org/10.1182/blood.v106.11.2714.2714.

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Abstract Core binding factors (CBFs) are heterodimers consisting of a DNA binding subunit (Runx1, Runx2, or Runx3) and a non-DNA binding CBFβ subunit. CBFβ increases the affinity of the Runx subunits for DNA. Embryos deficient for Runx1 or CBFβ die at midgestation with a complete failure of definitive hematopoiesis due to a block in hematopoietic stem cell (HSC) emergence. To examine the role of core binding factors at later stages of hematopoiesis, we generated a hypomorphic Cbfb allele (Cbfbrss), that when carried over a Cbfb null allele (Cbfbrss/−) results in a 3-4 fold reduction in CBFβ pr
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29

Jaffray, E., K. M. Wood, and R. T. Hay. "Domain organization of I kappa B alpha and sites of interaction with NF-kappa B p65." Molecular and Cellular Biology 15, no. 4 (1995): 2166–72. http://dx.doi.org/10.1128/mcb.15.4.2166.

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The DNA-binding activity and cellular distribution of the transcription factor NF-kappa B are regulated by the inhibitor protein I kappa B alpha. I kappa B alpha belongs to a family of proteins that contain multiple repeats of a 30- to 35-amino-acid sequence that was initially recognized in the erythrocyte protein ankyrin. Partial proteolysis has been used to study the domain structure of I kappa B alpha and to determine the sites at which it interacts with NF-kappa B. The data reveal a tripartite structure for I kappa B alpha in which a central, protease-resistant domain composed of five anky
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30

Hel, Z., E. Skamene, and D. Radzioch. "Two distinct regions in the 3' untranslated region of tumor necrosis factor alpha mRNA form complexes with macrophage proteins." Molecular and Cellular Biology 16, no. 10 (1996): 5579–90. http://dx.doi.org/10.1128/mcb.16.10.5579.

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The production of tumor necrosis factor alpha (TNF-alpha), a key proinflammatory cytokine essential for the function of the immune system, is regulated at both the transcriptional and posttranscriptional levels. In this report, we focus on the interaction of TNF-alpha mRNA with macrophage proteins, likely mediators of its post-transcriptional control. Mapping of murine TNF-alpha mRNA by using a combination of RNase protection and RNA gel shift assays revealed that two distinct sites within the 3' untranslated region (3'-UTR) engage in the formation of four major RNA-protein complexes, while no
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31

Weiss, M., C. Yokoyama, Y. Shikama, C. Naugle, B. Druker, and CA Sieff. "Human granulocyte-macrophage colony-stimulating factor receptor signal transduction requires the proximal cytoplasmic domains of the alpha and beta subunits." Blood 82, no. 11 (1993): 3298–306. http://dx.doi.org/10.1182/blood.v82.11.3298.3298.

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Abstract Human granulocyte-macrophage colony-stimulating factor (GM-CSF) controls the production, maturation, and function of cells in multiple hematopoietic lineages. These effects are mediated by a cell-surface receptor (GM-R) composed of alpha and beta subunits, each containing 378 and 881 amino acids, respectively. Whereas the alpha subunit exists as several isoforms that bind GM-CSF with low affinity, the beta common subunit (beta c) does not bind GM-CSF itself, but acts as a high- affinity converter for GM-CSF, interleukin-3 (IL-3), and IL-5 receptor alpha subunits. The cytoplasmic regio
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32

Weiss, M., C. Yokoyama, Y. Shikama, C. Naugle, B. Druker, and CA Sieff. "Human granulocyte-macrophage colony-stimulating factor receptor signal transduction requires the proximal cytoplasmic domains of the alpha and beta subunits." Blood 82, no. 11 (1993): 3298–306. http://dx.doi.org/10.1182/blood.v82.11.3298.bloodjournal82113298.

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Human granulocyte-macrophage colony-stimulating factor (GM-CSF) controls the production, maturation, and function of cells in multiple hematopoietic lineages. These effects are mediated by a cell-surface receptor (GM-R) composed of alpha and beta subunits, each containing 378 and 881 amino acids, respectively. Whereas the alpha subunit exists as several isoforms that bind GM-CSF with low affinity, the beta common subunit (beta c) does not bind GM-CSF itself, but acts as a high- affinity converter for GM-CSF, interleukin-3 (IL-3), and IL-5 receptor alpha subunits. The cytoplasmic region of GM-R
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33

Miyajima, I., L. Levitt, T. Hara, et al. "The murine interleukin-3 receptor alpha subunit gene: chromosomal localization, genomic structure, and promoter function." Blood 85, no. 5 (1995): 1246–53. http://dx.doi.org/10.1182/blood.v85.5.1246.bloodjournal8551246.

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The interleukin-3 receptor (IL-3R) is composed of alpha and beta subunits, members of the class I cytokine receptor family. Here we describe isolation and characterization of the chromosomal gene for the mouse IL-3R alpha subunit (mIL-3R alpha). Whereas the human IL-3R alpha gene is tightly linked with the granulocyte-macrophage colony- stimulating factor receptor alpha subunit (GM-CSFR alpha) gene in the pseudoautosomal region of the X and Y chromosomes, the mIL-3R alpha gene (II3ra) is located in the proximal region of mouse chromosome 14, separated from the mouse GM-CSFR alpha gene, which i
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34

Bhutada, A., and F. Ismail-Beigi. "Serum and growth factor induction of Na(+)-K(+)-ATPase subunit mRNAs in Clone 9 cells: role of protein kinase C." American Journal of Physiology-Cell Physiology 261, no. 4 (1991): C699—C707. http://dx.doi.org/10.1152/ajpcell.1991.261.4.c699.

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In a previous study, we found that addition of serum to confluent Clone 9 cells, a nontransformed rat liver cell line, increased the abundance of mRNA alpha 1 and mRNA beta 1 at 3 h by 2- and 2.7-fold, respectively [Bhutada et al. Am. J. Physiol. 258 (Cell Physiol. 27): C1044-C1050, 1990]. We now report that exposure of these cells to 160 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) for 6 h increases mRNA alpha 1 and mRNA beta 1 by 1.7 +/- 0.2- and 2.1 +/- 0.3-fold, respectively. Incubation in the presence of 160 nM TPA for 24 h reduced high-affinity phorbol dibutyrate-binding sites [dissocia
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35

Wang, S., Q. Wang, B. E. Crute, I. N. Melnikova, S. R. Keller, and N. A. Speck. "Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor." Molecular and Cellular Biology 13, no. 6 (1993): 3324–39. http://dx.doi.org/10.1128/mcb.13.6.3324.

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Moloney murine leukemia virus causes thymic leukemias when injected into newborn mice. A major determinant of the thymic disease specificity of Moloney virus genetically maps to the conserved viral core motif in the Moloney virus enhancer. Point mutations introduced into the core site significantly shifted the disease specificity of the Moloney virus from thymic leukemia to erythroid leukemia (N.A. Speck, B. Renjifo, E. Golemis, T.N. Fredrickson, J.W. Hartley, and N. Hopkins, Genes Dev. 4:233-242, 1990). We previously reported the purification of core-binding factors (CBF) from calf thymus nuc
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36

Wang, S., Q. Wang, B. E. Crute, I. N. Melnikova, S. R. Keller, and N. A. Speck. "Cloning and characterization of subunits of the T-cell receptor and murine leukemia virus enhancer core-binding factor." Molecular and Cellular Biology 13, no. 6 (1993): 3324–39. http://dx.doi.org/10.1128/mcb.13.6.3324-3339.1993.

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Moloney murine leukemia virus causes thymic leukemias when injected into newborn mice. A major determinant of the thymic disease specificity of Moloney virus genetically maps to the conserved viral core motif in the Moloney virus enhancer. Point mutations introduced into the core site significantly shifted the disease specificity of the Moloney virus from thymic leukemia to erythroid leukemia (N.A. Speck, B. Renjifo, E. Golemis, T.N. Fredrickson, J.W. Hartley, and N. Hopkins, Genes Dev. 4:233-242, 1990). We previously reported the purification of core-binding factors (CBF) from calf thymus nuc
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37

Takaki, S., Y. Murata, T. Kitamura, A. Miyajima, A. Tominaga, and K. Takatsu. "Reconstitution of the functional receptors for murine and human interleukin 5." Journal of Experimental Medicine 177, no. 6 (1993): 1523–29. http://dx.doi.org/10.1084/jem.177.6.1523.

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The murine interleukin 5 receptor (mIL-5R) is composed of two distinct subunits, alpha and beta. The alpha subunit (mIL-5R alpha) specifically binds IL-5 with low affinity. The beta subunit (mIL-5R beta) does not bind IL-5 by itself, but forms the high-affinity receptor with mIL-5R alpha. mIL-5R beta has been revealed to be the mIL-3R-like protein, AIC2B which is shared with receptors for IL-3 and granulocyte/macrophage colony-stimulating factor. We demonstrated here the reconstitution of the functional receptors for murine and human IL-5 on the mouse IL-2-dependent cell line, CTLL-2. CTLL-2 w
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38

O'Brien, R. M., E. L. Noisin, A. Suwanichkul, et al. "Hepatic nuclear factor 3- and hormone-regulated expression of the phosphoenolpyruvate carboxykinase and insulin-like growth factor-binding protein 1 genes." Molecular and Cellular Biology 15, no. 3 (1995): 1747–58. http://dx.doi.org/10.1128/mcb.15.3.1747.

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The rate of transcription of the hepatic phosphoenolpyruvate carboxykinase (PEPCK) and insulin-like growth factor-binding protein 1 (IGFBP-1) genes is stimulated by glucocorticoids and inhibited by insulin. In both cases, the effect of insulin is dominant, since it suppresses both basal and glucocorticoid-stimulated PEPCK or IGFBP-1 gene transcription. Analyses of both promoters by transfection of PEPCK or IGFBP-1-chloramphenicol acetyltransferase fusion genes into rat hepatoma cells has led to the identification of insulin response sequences (IRSs) in both genes. The core IRS, T(G/A)TTTTG, is
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39

Cockell, M., D. Stolarczyk, S. Frutiger, G. J. Hughes, O. Hagenbüchle, and P. K. Wellauer. "Binding sites for hepatocyte nuclear factor 3 beta or 3 gamma and pancreas transcription factor 1 are required for efficient expression of the gene encoding pancreatic alpha-amylase." Molecular and Cellular Biology 15, no. 4 (1995): 1933–41. http://dx.doi.org/10.1128/mcb.15.4.1933.

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Efficient expression of genes under the control of alpha-amylase 2 5'-flanking sequences in exocrine pancreatic cells requires, in addition to the pancreas transcription factor 1 binding site (M. Cockell, B.J. Stevenson, M. Strubin, O. Hagenbüchle, and P. K. Wellauer, Mol. Cell. Biol. 9:2464-2476, 1989), another cis-acting element at positions -60 to -86. This DNA element, which contains an AT-rich core, site for nuclear proteins present not only in the pancreas but also in other tissues and cell lines derived from the endoderm. Purification of binding activities from pancreatic cells by DNA a
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40

Muraoka, A., M. Kaise, Y. J. Guo, et al. "Canine H(+)-K(+)-ATPase alpha-subunit gene promoter: studies with canine parietal cells in primary culture." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 6 (1996): G1104—G1113. http://dx.doi.org/10.1152/ajpgi.1996.271.6.g1104.

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H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase) is the principal enzyme responsible for the process of gastric acid secretion. This enzyme is expressed in a cell-type-specific manner in gastric parietal cells. To explore the mechanisms regulating its expression, we transfected differentiated canine parietal cells in primary culture with H(+)-K(+)-ATPase-luciferase reporter genes and assessed transcriptional activities. Deletional analysis of the 5'-flanking region of this gene demonstrated a remarkable increment in transcriptional activity associated with a segment between bases -54 to -4
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41

Gout, I., R. Dhand, G. Panayotou та ін. "Expression and characterization of the p85 subunit of the phosphatidylinositol 3-kinase complex and a related p85β protein by using the baculovirus expression system". Biochemical Journal 288, № 2 (1992): 395–405. http://dx.doi.org/10.1042/bj2880395.

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PtdIns 3-kinase associates with certain activated protein-tyrosine kinase receptors and with the pp60c-src/polyoma middle-T complex, suggesting that the enzyme is involved in growth regulation. The purified PtdIns 3-kinase appears to have two subunits, of 85 kDa and 110 kDa. Structural analysis at protein and cDNA levels revealed two forms of the 85 kDa subunit, one which associates with PtdIns 3-kinase activity termed p85 alpha, and a protein of unknown function, p85 beta. Both 85 kDa proteins contain src-homology regions 2 and 3 (SH2 and SH3), but lack enzymic activity, suggesting that they
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42

Cooper, J. A., and A. Kashishian. "In vivo binding properties of SH2 domains from GTPase-activating protein and phosphatidylinositol 3-kinase." Molecular and Cellular Biology 13, no. 3 (1993): 1737–45. http://dx.doi.org/10.1128/mcb.13.3.1737.

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We have used a transient expression system and mutant platelet-derived growth factor (PDGF) receptors to study the binding specificities of the Src homology 2 (SH2) regions of the Ras GTPase-activator protein (GAP) and the p85 alpha subunit of phosphatidylinositol 3-kinase (PI3 kinase). A number of fusion proteins, each tagged with an epitope allowing recognition by a monoclonal antibody, were expressed at levels comparable to those of endogenous GAP. Fusion proteins containing the central SH2-SH3-SH2 region of GAP or the C-terminal region of p85 alpha, which includes two SH2 domains, bound to
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43

Cooper, J. A., and A. Kashishian. "In vivo binding properties of SH2 domains from GTPase-activating protein and phosphatidylinositol 3-kinase." Molecular and Cellular Biology 13, no. 3 (1993): 1737–45. http://dx.doi.org/10.1128/mcb.13.3.1737-1745.1993.

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We have used a transient expression system and mutant platelet-derived growth factor (PDGF) receptors to study the binding specificities of the Src homology 2 (SH2) regions of the Ras GTPase-activator protein (GAP) and the p85 alpha subunit of phosphatidylinositol 3-kinase (PI3 kinase). A number of fusion proteins, each tagged with an epitope allowing recognition by a monoclonal antibody, were expressed at levels comparable to those of endogenous GAP. Fusion proteins containing the central SH2-SH3-SH2 region of GAP or the C-terminal region of p85 alpha, which includes two SH2 domains, bound to
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44

Li, Xianjing, Duowei Wang, Zhen Chen та ін. "Gαi1and Gαi3regulate macrophage polarization by forming a complex containing CD14 and Gab1". Proceedings of the National Academy of Sciences 112, № 15 (2015): 4731–36. http://dx.doi.org/10.1073/pnas.1503779112.

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Heterotrimeric G proteins have been implicated in Toll-like receptor 4 (TLR4) signaling in macrophages and endothelial cells. However, whether guanine nucleotide-binding protein G(i) subunit alpha-1 and alpha-3 (Gαi1/3) are required for LPS responses remains unclear, and if so, the underlying mechanisms need to be studied. In this study, we demonstrated that, in response to LPS, Gαi1/3form complexes containing the pattern recognition receptor (PRR) CD14 and growth factor receptor binding 2 (Grb2)-associated binding protein (Gab1), which are required for activation of PI3K-Akt signaling. Gαi1/3
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45

Benjamin, Bradley, Ana M. Sanchez, Angad Garg, Beate Schwer, and Stewart Shuman. "Structure-function analysis of fission yeast cleavage and polyadenylation factor (CPF) subunit Ppn1 and its interactions with Dis2 and Swd22." PLOS Genetics 17, no. 3 (2021): e1009452. http://dx.doi.org/10.1371/journal.pgen.1009452.

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Fission yeast Cleavage and Polyadenylation Factor (CPF), a 13-subunit complex, executes the cotranscriptional 3’ processing of RNA polymerase II (Pol2) transcripts that precedes transcription termination. The three-subunit DPS sub-complex of CPF, consisting of a PP1-type phosphoprotein phosphatase Dis2, a WD-repeat protein Swd22, and a putative phosphatase regulatory factor Ppn1, associates with the CPF core to form the holo-CPF assembly. Here we probed the functional, physical, and genetic interactions of DPS by focusing on the Ppn1 subunit, which mediates association of DPS with the core. Tr
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46

Gruel, Y., E. Brojer, D. J. Nugent, and T. J. Kunicki. "Further characterization of the thrombasthenia-related idiotype OG. Antiidiotype defines a novel epitope(s) shared by fibrinogen B beta chain, vitronectin, and von Willebrand factor and required for binding to beta 3." Journal of Experimental Medicine 180, no. 6 (1994): 2259–67. http://dx.doi.org/10.1084/jem.180.6.2259.

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A patient (OG) with Glanzmann thrombasthenia became refractory to platelet transfusion after the production of an immunoglobulin G (IgG) isoantibody (Ab1) specific for the integrin subunit beta 3. To determine the frequency at which the OG idiotype is found in the general population and in immune-mediated disease states, we developed a rabbit polyclonal antibody (Ab2) specific for affinity-purified OG anti-beta 3 Fab. The binding of Ab2 to Ab1 is inhibited by purified alpha IIb beta 3. Ab2 als binds to IgG specific for alpha IIb beta 3 obtained from one nonrelated Glanzmann thrombasthenia pati
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47

Denis, C., JA Williams, X. Lu, D. Meyer, and D. Baruch. "Solid-phase von Willebrand factor contains a conformationally active RGD motif that mediates endothelial cell adhesion through the alpha v beta 3 receptor." Blood 82, no. 12 (1993): 3622–30. http://dx.doi.org/10.1182/blood.v82.12.3622.3622.

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Abstract The interaction of von Willebrand factor (vWF) with the alpha v beta 3 integrin of human umbilical vein endothelial cells is dependent on the RGD sequence present at residues 1744–1746 of the mature vWF subunit. We compared vWF and its two dimeric fragments, SpIII (residues 1–1365) and SpII (residues 1366–2050), as adhesion substrates. Solid-phase vWF and SpII supported endothelial cell adhesion, whereas SpIII, which contains the glycoprotein (GP) Ib binding domain, did not. Soluble SpII inhibited adhesion to immobilized ligands, whereas soluble vWF did not, suggesting that exposure o
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48

Denis, C., JA Williams, X. Lu, D. Meyer, and D. Baruch. "Solid-phase von Willebrand factor contains a conformationally active RGD motif that mediates endothelial cell adhesion through the alpha v beta 3 receptor." Blood 82, no. 12 (1993): 3622–30. http://dx.doi.org/10.1182/blood.v82.12.3622.bloodjournal82123622.

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The interaction of von Willebrand factor (vWF) with the alpha v beta 3 integrin of human umbilical vein endothelial cells is dependent on the RGD sequence present at residues 1744–1746 of the mature vWF subunit. We compared vWF and its two dimeric fragments, SpIII (residues 1–1365) and SpII (residues 1366–2050), as adhesion substrates. Solid-phase vWF and SpII supported endothelial cell adhesion, whereas SpIII, which contains the glycoprotein (GP) Ib binding domain, did not. Soluble SpII inhibited adhesion to immobilized ligands, whereas soluble vWF did not, suggesting that exposure of the cel
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49

Fry, M. J., G. Panayotou, R. Dhand, et al. "Purification and characterization of a phosphatidylinositol 3-kinase complex from bovine brain by using phosphopeptide affinity columns." Biochemical Journal 288, no. 2 (1992): 383–93. http://dx.doi.org/10.1042/bj2880383.

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Specific phosphorylated tyrosine residues in the kinase insert region of the human platelet-derived-growth-factor beta-receptor mediate the formation of multienzyme complexes with this receptor. When phosphorylated, tyrosine residue 751 within the kinase insert region mediates binding of PtdIns 3-kinase to this receptor. A 17-amino-acid peptide containing this tyrosine residue was synthesized, phosphorylated by using epidermal-growth-factor receptor and then coupled to an Actigel matrix. The tyrosine-751 phosphopeptide column is used here as a final affinity step in the purification of the Ptd
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50

McLeish, K. R., J. B. Klein, T. Schepers та G. Sonnenfeld. "Modulation of transmembrane signalling in HL-60 granulocytes by tumour necrosis factor-α". Biochemical Journal 279, № 2 (1991): 455–60. http://dx.doi.org/10.1042/bj2790455.

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Differentiated HL-60 granulocytes were used to study the mechanism by which tumour necrosis factor-alpha (TNF) enhances responses to N-formyl-methionyl-leucylphenylalanine (FMLP). Cultivation of differentiated HL-60 cells with 100 units of TNF/ml for 24 h resulted in a 3-fold increase in superoxide release and 4-fold increase in prostaglandin E2 production on stimulation with 1 microM-FMLP. On the other hand, cultivation with TNF failed to increase phorbol diester stimulation of superoxide release. Formyl-peptide-receptor expression determined on isolated membranes from cells cultivated with T
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