Relevant bibliographies by topics / CREBBP

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'CREBBP'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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Journal articles on the topic "CREBBP"

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Yu, Chuanjiang, Mara Holloman, Andrew Kim, et al. "Differential Role of Crebbp Missense and Truncating Mutations in the Malignant Transformation of Germinal Center B Cells." Blood 144, Supplement 1 (2024): 47. https://doi.org/10.1182/blood-2024-208876.

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Somatic mutations of the CREBBP acetyltransferase are highly recurrent in germinal center (GC)-derived lymphomas, including follicular lymphoma (FL, 60% of cases) and diffuse large B cell lymphoma (DLBCL; 40% of cases in the EZB/C3 genetic subtype). Mutations include prototypical inactivating events that abrogate the C-terminal acetyltransferase (AT) domain, as well as amino-acid changes clustering within this domain, which impair the protein enzymatic activity by decreasing its affinity for acetyl-coenzyme A (Pasqualucci et al., Nature 2011). These events are acquired early during lymphomagen
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Meyer, Stefanie, Sofija Vlasevska, Laura Garcia Ibanez, Claudio Scuoppo, Riccardo Dalla-Favera, and Laura Pasqualucci. "Targeting Histone Acetyltransferase Gene Inactivation in Diffuse Large B Cell Lymphoma." Blood 132, Supplement 1 (2018): 671. http://dx.doi.org/10.1182/blood-2018-99-117542.

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Abstract Diffuse Large B-cell Lymphoma (DLBCL) is the most common form of non-Hodgkin lymphoma, accounting for ~30% of de-novo diagnoses and also arising as a frequent clinical evolution of indolent lymphomas. Although curable in a substantial fraction of cases, one third of patients do not achieve durable remissions, highlighting the need for novel, targeted therapies. Over the past decade, we and others have identified the CREBBP acetyltransferase and, less frequently, its paralogue EP300 as highly recurrent targets of inactivating somatic mutations/deletions in DLBCL and follicular lymphoma
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Ying, Hsia-Yuan, Yanwen Jiang, Ana Ortega-Molina, et al. "Crebbp Mutations Disrupt Dynamic Enhancer Acetylation in B-Cells, Enabling HDAC3 to Drive Lymphomagenesis." Blood 128, no. 22 (2016): 735. http://dx.doi.org/10.1182/blood.v128.22.735.735.

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Abstract Somatic mutations in CREBBP occur frequently in germinal center derived lymphomas such as DLBCL and FL. However whether or how these mutations might contribute to lymphomagenesis is still largely unknown. Most CREBBP mutations are predicted to result in loss of function since they target the histone acetyltransferase (HAT) domain or give rise to premature stop codon prior to the HAT domain. Here, we show that Crebbp shRNA knockdown (KD) accelerated lymphomagenesis in VavP-Bcl2 transgenic mice, a model that recapitulates human GC-derived lymphomas. The median time to lymphoma onset in
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LeBlanc, Francis, Josh Bennett, Kwangmin Choi, and Daniel T. Starczynowski. "Targeting CREB-Binding Protein (CREBBP) Overcomes Resistance to Azacitidine and Venetoclax Therapy in Acute Myeloid Leukemia (AML)." Blood 142, Supplement 1 (2023): 5765. http://dx.doi.org/10.1182/blood-2023-187063.

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Acute myeloid leukemia (AML) is a clonal myeloid malignancy arising from hematopoietic stem or progenitor cells (HSPC) within the bone marrow (BM). Despite advancements in our understanding of AML pathogenesis, patients continue to face grim outcomes, with a five-year relative survival rate of approximately 20%. This highlights the pressing need to identify molecular features of AML that are amenable to therapeutic intervention. The ideal molecular targets would be those broadly dysregulated and integral to multiple signaling pathways implicated in AML pathogenesis. Recent therapeutic regimens
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Lamble, Adam J., Robert B. Gerbing, Jenny L. Smith, et al. "Crebbp Alterations Are Associated with a Poor Prognosis in De Novo AML." Blood 138, Supplement 1 (2021): 3451. http://dx.doi.org/10.1182/blood-2021-154052.

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Abstract Introduction: The translocation, t(8;16)(p11;p13), results in the fusion between KAT6A and CREBBP and has been associated with a poor prognosis in both pediatric and adult acute myeloid leukemia (AML). This lesion has therefore been re-classified as high risk on the active Phase 3 Children's Oncology Group (COG) trial for de novo AML, AAML1831 (NCT04293562). Less is known about the prognostic significance of CREBBP sequence variants. Methods: CREBBP variant status was determined in patients with AML enrolled on 4 successive COG trials for de novo pediatric AML (NCT00003790, NCT0007017
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Zhu, Yu, Zi Wang, Yanan Li, et al. "The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies." Cancers 15, no. 4 (2023): 1219. http://dx.doi.org/10.3390/cancers15041219.

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Disordered histone acetylation has emerged as a key mechanism in promoting hematological malignancies. CREB-binding protein (CREBBP) and E1A-binding protein P300 (EP300) are two key acetyltransferases and transcriptional cofactors that regulate gene expression by regulating the acetylation levels of histone proteins and non-histone proteins. CREBBP/EP300 dysregulation and CREBBP/EP300-containing complexes are critical for the initiation, progression, and chemoresistance of hematological malignancies. CREBBP/EP300 also participate in tumor immune responses by regulating the differentiation and
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Hashwah, Hind, Corina A. Schmid, Sabrina Kasser, et al. "Inactivation of CREBBP expands the germinal center B cell compartment, down-regulates MHCII expression and promotes DLBCL growth." Proceedings of the National Academy of Sciences 114, no. 36 (2017): 9701–6. http://dx.doi.org/10.1073/pnas.1619555114.

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The genes encoding the histone acetyl-transferases (HATs) CREB binding protein (CREBBP) and EP300 are recurrently mutated in the activated B cell-like and germinal center (GC) B cell-like subtypes of diffuse large B cell lymphoma (DLBCL). Here, we introduced a patient mutation into a human DLBCL cell line using CRISPR and deleted Crebbp and Ep300 in the GC B cell compartment of mice. CREBBP-mutant DLBCL clones exhibited reduced histone H3 acetylation, expressed significantly less MHCII, and grew faster than wild-type clones in s.c. and orthotopic xenograft models. Mice lacking Crebbp in GC B c
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Zimmer, Stephanie N., Qing Zhou, Ting Zhou, et al. "Crebbp haploinsufficiency in mice alters the bone marrow microenvironment, leading to loss of stem cells and excessive myelopoiesis." Blood 118, no. 1 (2011): 69–79. http://dx.doi.org/10.1182/blood-2010-09-307942.

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Abstract CREB-binding protein (CREBBP) is important for the cell-autonomous regulation of hematopoiesis, including the stem cell compartment. In the present study, we show that CREBBP plays an equally pivotal role in microenvironment-mediated regulation of hematopoiesis. We found that the BM microenvironment of Crebbp+/− mice was unable to properly maintain the immature stem cell and progenitor cell pools. Instead, it stimulates myeloid differentiation, which progresses into a myeloproliferation phenotype. Alterations in the BM microenvironment resulting from haploinsufficiency of Crebbp inclu
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Huntly, Brian J. P., Sarah Jayne Horton, George Giotopoulos, et al. "Early Loss of CREBBP Confers Malignant Stem Cell Properties on Lymphoid Progenitors." Blood 128, no. 22 (2016): 460. http://dx.doi.org/10.1182/blood.v128.22.460.460.

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Abstract Loss-of-function mutations of the cyclic-AMP response element binding protein, binding protein (CREBBP) gene have recently been described at high frequencies across a spectrum of lymphoid malignancies, particularly follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL). The multiple effects of this epigenetic regulator on developmental and homeostatic processes have been extensively studied, however, exactly how CREBBP functions as a tumor suppressor and the reasons for its particular predilection for suppression of lymphoid tumors remains unclear. In addition, for many ma
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Peck, Barrie, Philip Bland, Ionnana Mavrommati, et al. "3D functional genomics screens identify CREBBP as a targetable driver in aggressive triple-negative breast cancer." Cancer Res 81, no. 4 (2021): 847–59. https://doi.org/10.1158/0008-5472.CAN-20-1822.

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Triple-negative breast cancers (TNBC) are resistant to standard-of-care chemotherapy and lack known targetable driver gene alterations. Identification of novel drivers could aid the discovery of new treatment strategies for this hard-to-treat patient population, yet studies using high-throughput and accurate models to define the functions of driver genes in TNBC to date have been limited. Here, we employed unbiased functional genomics screening of the 200 most frequently mutated genes in breast cancer, using spheroid cultures to model&nbsp;<em>in vivo</em>&ndash;like conditions, and identified
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Dissertations / Theses on the topic "CREBBP"

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Dixon, Zach Adam. "The role of CREBBP mutations in lymphoid malignancies." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3556.

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Relapsed acute lymphoblastic leukaemia (ALL), diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) comprise a group of malignancies with poor prognosis and therapeutic strategies are needed to improve outcomes. Recent studies have shown that heterozygous inactivating mutations in the histone acetyl transferase, CREBBP, are frequent in these malignancies, and are thought to lead to impaired transcription of glucocorticoid (GC) response genes. Given the pivotal role of GC in the treatment of lymphoid malignancies and the finding that CREBBP mutations often arise at relapse, it has
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Dawes, Joanna Camilla. "Modelling Crebbp loss in BCL2 driven non-Hodgkin's lymphoma." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/58194.

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Non-Hodgkin’s lymphomas (NHL) are a spectrum of hematopoietic cancer accounting for 4% of new cancer diagnoses each year. Approximately 95% of all NHL are of B-cell origin; diffuse large B-cell lymphomas (DLBCL) and follicular lymphoma (FL) accounting for 30-40% and 20% of B-NHL respectively. Recent human mutation profiling and resequencing studies have shown that CREBBP and BCL2 are frequently mutated, early events in B-NHL that are often are concurrent. This thesis presents a study of their role in oncogenesis by generating a novel model of B-NHL overexpressing BCL2 in the haematopoetic comp
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BENTIVEGNA, ANGELA. "Ricerca di alterazioni del Gene CREBBP (CREB Binding Protein) in pazienti con sindrome di Rubinstein-Taybi." Bachelor's thesis, Università degli Studi di Milano-Bicocca, 2004. http://hdl.handle.net/10281/12824.

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Di, Dio Laura Giusy Rosaria Agata. "Sindrome da microduplicazione 16p13.3 espansione del fenotipo." Doctoral thesis, Università di Catania, 2012. http://hdl.handle.net/10761/1062.

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Le sindromi da microalterazione cromosomica sono sindromi costituzionali con ritardo mentale e anomalie fenotipiche multiple causate da sbilanci di specifiche regioni del genoma. Se il riarrangiamento cromosomico include poche megabasi viene detto criptico perché spesso non è diagnosticabile con un esame cromosomico convenzionale. Per molti anni, tuttavia, cioè fino a quando è stata disponibile solo la tecnica tradizionale e FISH per l analisi di cromosomi metafasici, erano conosciute soltanto le microdelezioni delle regioni fiancheggiate da dupliconi. La mancata diagnosi citogenetica-molec
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BENTIVEGNA, ANGELA. "Base molecolare della sindrome di Chromatin remodelling Rubinstein-Taybi: un sistema modello per lo studio dei deficit funzionali di acetilazione istonica." Doctoral thesis, Università degli studi di Milano, 2008. http://hdl.handle.net/10281/12823.

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Rubinstein–Taybi syndrome (RSTS) is a rare malformation disorder caused by mutations in the closely related CREBBP and EP300 genes, accounting respectively for up to 60 and 3% of cases. About 10% of CREBBP mutations are whole gene deletions often extending into flanking regions. Using FISH and microsatellite analyses as a first step in the CREBBP mutation screening of 63 Italian RSTS patients (pts), 6 deletions were identified, 3 of which were in a mosaic condition that has not been previously reported in RSTS. The clinical presentation was typical in all cases, but more severe in the three pt
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Camós, Guijosa Mireia. "Caracterización biológica de la leucemia mieloide aguda con translocación t(8;16)(p11;p13) y reordenamiento MYST3-CREBBP." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/2220.

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INTRODUCCIÓN. La leucemia mieloide aguda (LMA) es una enfermedad heterogénea desde el punto de vista clínico y biológico. En los últimos años se vienen reconociendo diversas alteraciones moleculares que definen entidades específicas. En este contexto, la LMA con translocación t(8;16)(p11;p13) y reordenamiento MYST3 (MOZ)/CREBBP (CBP) es una variedad infrecuente mal caracterizada desde el punto de vista biológico. <br/><br/>HIPÓTESIS Y OBJETIVOS. La proteína quimérica MYST3-CREBBP, resultante de la translocación t(8;16)(p11;p13), podría conferir a este subtipo de LMA una individualidad biológic
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Torres, Leuridan Cavalcante. "Avaliação da imunocompetência de portadores da síndrome de Rubinstein-taybi." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-01092008-192345/.

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A síndrome de Rubinstein-Taybi (RTS, OMIM 180849) é uma doença autossômica dominante caracterizada por dismorfismos craniofaciais típicos, polegares e háluces alargados, infecções respiratórias recidivantes, retardo mental e de crescimento. RTS está associada com mutação no gene CREBBP. Na avaliação da imunocompetência de 17 portadores de RTS, observaram-se algumas alterações na resposta imune inata e adaptativa: leucocitose persistente, neutrófilos com desgranulopoiese, elevada concentração sérica de IgM e IgG1, produção normal de anticorpos contra antígenos protéicos e anti-polissacarídeos,
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Djavanroodi, Faramarz. "Creep and creep-fracture crack growth." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47412.

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Whitt, Harrison Collin. "Creep and Creep-fatigue Deformation Studies in 22V and P91 Creep-strength EnhancedFerritic Steels." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1555603135480185.

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Giannopoulos, Ioannis. "Creep and creep-rupture behaviour of Aramid fibres." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/252181.

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To obtain creep-rupture data at low level within a reasonably short time-scale, two accelerated techniques have been investigated. Stepped Isothermal Method (SIM) testing involves loading a single specimen, under constant load, with the temperature increased in a series of steps to accelerate the creep. Careful choice of the temperature step and step duration allow the test to be completed in about 24 hours. At each temperature step a creep curve is obtained; these are then adjusted to compensate for the different temperature levels and a creep master curve at a reference temperature is produc
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Books on the topic "CREBBP"

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Johanknecht, Susan. Creep. Gefn Press, 1997.

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de, Villiers H. L., ed. The physics of creep: Creep and creep-resistant alloys. Taylor & Francis, 1995.

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Betten, Josef. Creep Mechanics. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04971-6.

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Battin, B. W. The Creep. Fawcett Gold Medal, 1986.

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service), SpringerLink (Online, ed. Creep Mechanics. Springer-Verlag Berlin Heidelberg, 2008.

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Pelham, David. Crawlies creep. Dutton, 1996.

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Battin, B. W. The Creep. Fawcett Gold Medal, 1986.

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Merritt, A. Creep, Shadow, Creep. Independently Published, 2021.

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Merritt, A. Creep, Shadow, Creep. Independently Published, 2018.

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Merritt, A. Creep, Shadow, Creep. Independently Published, 2019.

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Book chapters on the topic "CREBBP"

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Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, Gen Nishimura, and Valérie Cormier-Daire. "Rubinstein-Taybi Syndrome, CREBBP- and EP300-Related." In Fetal and Perinatal Skeletal Dysplasias, 2nd ed. CRC Press, 2024. http://dx.doi.org/10.1201/9781003166948-61.

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Razdolsky, Leo. "Peculiarities of Phenomenological Models of Nanocomposites." In Creep. CRC Press, 2023. http://dx.doi.org/10.1201/9781003267720-4.

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Razdolsky, Leo. "Phenomenological Creep-Fatigue Models." In Creep. CRC Press, 2023. http://dx.doi.org/10.1201/9781003267720-3.

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Razdolsky, Leo. "Cumulative Damage Model (CDM) of Cyclic Creep-Fatigue Process." In Creep. CRC Press, 2023. http://dx.doi.org/10.1201/9781003267720-2.

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Razdolsky, Leo. "Probabilistic Approach to Creep-Fatigue Models." In Creep. CRC Press, 2023. http://dx.doi.org/10.1201/9781003267720-5.

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Razdolsky, Leo. "Introduction and Assumptions." In Creep. CRC Press, 2023. http://dx.doi.org/10.1201/9781003267720-1.

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Sandström, Rolf. "Creep with Low Stress Exponents." In Basic Modeling and Theory of Creep of Metallic Materials. Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-49507-6_5.

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AbstractPrimary creep models predict that at low stresses a stress exponent of 1 can be obtained for dislocation creep. Also experimentally this has been observed for an austenitic stainless steel. The time dependence of the primary creep verifies that it is dislocation creep. An other example is for Al at very high temperatures (Harper-Dorn creep), where at sufficiently low stresses, the stress exponent approaches 1. For both materials higher stresses give larger stress exponents as expected for dislocation creep. Obviously, diffusion and dislocation creep can be competing processes. The vali
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Sandström, Rolf. "Primary Creep." In Basic Modeling and Theory of Creep of Metallic Materials. Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-49507-6_4.

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AbstractFor many materials, primary creep can be described with the phi (ϕ) model and tertiary creep with the Omega (Ω) model (discussed in Chap. 12). According to the phi model, the creep rate is linear in strain and time in a double logarithmic diagram. When using empirical descriptions of the creep curves, these models are recommended. Several basic models for primary creep are derived. They are based on the creep rate in the secondary stage. This means that primary creep can be derived without any new data. The primary creep models are in agreement with the phi model and can describe exper
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John, Vernon. "Creep and Creep Testing." In Testing of Materials. Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-21969-8_7.

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Migoń, Piotr. "Creep." In Encyclopedia of Natural Hazards. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-1-4020-4399-4_79.

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Conference papers on the topic "CREBBP"

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Green, Michael R. "Abstract IA25: CREBBP: Not all mutations are created equal." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-ia25.

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"Анализ молекулярных последовательностей гена CREBBP методом главных компонент (PCA-seq)". У Биоинформатика регуляции и структуры геномов / системная биология. ИЦиГ СО РАН, 2024. http://dx.doi.org/10.18699/bgrs2024-9.1-06.

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Chang, Yunchao, David W. Woessner, Wenwei Lin, et al. "Abstract IA12: Modeling and targeting CREBBP mutations in relapsed acute lymphoblastic leukemia." In Abstracts: AACR Special Conference: Pediatric Cancer Research: From Basic Science to the Clinic; December 3-6, 2017; Atlanta, Georgia. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.pedca17-ia12.

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Zhou, Ting, Ziming Cheng, Christi Walter, and Vivienne I. Rebel. "Abstract B27: Novel insights into the pathogenesis of myelodysplastic syndrome using Crebbp+/- mice." In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-b27.

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Pickering, Curtis, Manish Kumar, Kathleen Bridges, et al. "Abstract 2925: Targeting histone acetyltransferase (HAT) function for synthetic cytotoxicity in CREBBP/EP300 mutant tumors." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2925.

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Pickering, Curtis, Manish Kumar, Kathleen Bridges, et al. "Abstract 2925: Targeting histone acetyltransferase (HAT) function for synthetic cytotoxicity in CREBBP/EP300 mutant tumors." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2925.

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Peck, Barrie, Philip J. Bland, Patty T. Wai, et al. "Abstract 788: Modeling tumor microenvironmental heterogeneity identifies CREBBP as a novel tumor suppressor in breast cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-788.

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Li, Jiaping, Wenzhe Fan, Yue Zhao, et al. "Abstract 2236: A Pan-cancer Analysis of CREBBP as a potential predictor for immune checkpoint therapy." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2236.

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Natrajan, Rachael. "Abstract P3-10-17: CREBBP alterations lead to CDK4/6 inhibitor sensitivity in triple negative breast cancer." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-10-17.

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Kumar, Manish, Kathleen Bridges, David Molkentine, et al. "Abstract 978: In vivo shRNA screening identifies synthetic cytotoxicity in CREBBP/EP300 mutant head and neck cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-978.

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Reports on the topic "CREBBP"

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Brenkus, Natassia, Garrett Tatum, Pedram Ghassemi, and Lautaro Martinez. Creep and Shrinkage of Nonproprietary Ultra-High Performance Concrete. Precast/Prestressed Concrete Institute, 2023. http://dx.doi.org/10.15554/pci.rr.mat-014.

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Work to characterize the creep and shrinkage of UHPC has been mainly performed on proprietary or lab-formulated mixes; this report describes the first effort to characterize creep and shrinkage properties of UHPC mixes explicitly formulated for use in large-scale precast/prestressed operations. To provide better knowledge about UHPCs, the research group at The Ohio State University performed a comprehensive study on the creep and shrinkage behavior of five UHPC mixes developed for use in the precast/prestressed industry using non-proprietary, locally available materials. This report details th
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Bernstein. L51921 Evaluating the Remaining Creep Life of Gas Turbine Blades. Pipeline Research Council International, Inc. (PRCI), 2001. http://dx.doi.org/10.55274/r0011270.

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A study was performed on methods to determine the remaining creep life of gas turbine blades. The objective of the study was to develop a remaining creep life methodology that will allow greater life to be obtained from these very expensive engine components. The focus of this study was on methods of physical testing, especially mechanical testing.
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Thembeka Ncube, Ayanda, and Antonio Bobet. Use of Recycled Asphalt. Purdue University, 2021. http://dx.doi.org/10.5703/1288284317316.

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The term Reclaimed Asphalt Pavement (RAP) is used to designate a material obtained from the removal of pavement materials. RAP is used across the US in multiple applications, largely on asphalt pavement layers. RAP can be described as a uniform granular non-plastic material, with a very low percentage of fines. It is formed by aggregate coated with a thin layer of asphalt. It is often used mixed with other granular materials. The addition of RAP to aggregates decreases the maximum dry unit weight of the mixture and decreases the optimum water content. It also increases the Resilient Modulus of
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Wright, Jill K., Laura J. Carroll, and Richard N. Wright. Creep and Creep-Fatigue of Alloy 617 Weldments. Office of Scientific and Technical Information (OSTI), 2014. http://dx.doi.org/10.2172/1168621.

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Zaheen Nasir, K., Wen Jiang, and Benjamin Spencer. Creep and Creep Fracture Modeling with Surrogate Creep Models and the Extended Finite Element Method. Office of Scientific and Technical Information (OSTI), 2024. https://doi.org/10.2172/2480345.

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Dr. F. W. Brust, Dr. G. M. Wilkowski, Dr. P. Krishnaswamy, and Mr. Keith Wichman. Creep and Creep-Fatigue Crack Growth at Structural Discontinuities and Welds. Office of Scientific and Technical Information (OSTI), 2010. http://dx.doi.org/10.2172/974286.

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Ubic, Rick, Darryl Butt, and William Windes. Irradiation Creep in Graphite. Office of Scientific and Technical Information (OSTI), 2014. http://dx.doi.org/10.2172/1128528.

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JL Bump and RF Luther. Biaxial Creep Specimen Fabrication. Office of Scientific and Technical Information (OSTI), 2006. http://dx.doi.org/10.2172/884675.

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Frank E. Goodwin. Creep Resistant Zinc Alloy. Office of Scientific and Technical Information (OSTI), 2002. http://dx.doi.org/10.2172/809087.

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Kennedy, C. R. (Irradiation creep of graphite). Office of Scientific and Technical Information (OSTI), 1990. http://dx.doi.org/10.2172/6410826.

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