Academic literature on the topic 'SAMD14'
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Journal articles on the topic "SAMD14"
Hewitt, Kyle J., Suhita Ray, Srinivas Chava, and Linda Chee. "The Samd14 Sterile Alpha Motif Domain Promotes Stress-Induced Cellular Signaling and Survival." Blood 134, Supplement_1 (November 13, 2019): 1184. http://dx.doi.org/10.1182/blood-2019-131228.
Full textRay, Suhita, Linda Chee, Daniel R. Matson, Nick Y. Palermo, Emery H. Bresnick, and Kyle J. Hewitt. "Sterile α-motif domain requirement for cellular signaling and survival." Journal of Biological Chemistry 295, no. 20 (April 2, 2020): 7113–25. http://dx.doi.org/10.1074/jbc.ra119.011895.
Full textRay, Suhita, Linda Chee, Nicholas T. Woods, and Kyle J. Hewitt. "Functional Requirements of a Samd14-Capping Protein Interaction in Stress Erythropoiesis." Blood 138, Supplement 1 (November 5, 2021): 288. http://dx.doi.org/10.1182/blood-2021-152898.
Full textHewitt, Kyle J. "The Samd14-Capping Protein Complex Controls Cell Signaling in the Erythropoietic Stress Response." Blood 136, Supplement 1 (November 5, 2020): 1. http://dx.doi.org/10.1182/blood-2020-143020.
Full textThurner, Lorenz, Klaus-Dieter Preuss, Moritz Bewarder, Maria Kemele, Natalie Fadle, Evi Regitz, Sarah Altmeyer, et al. "Hyper-N-glycosylated SAMD14 and neurabin-I as driver autoantigens of primary central nervous system lymphoma." Blood 132, no. 26 (December 27, 2018): 2744–53. http://dx.doi.org/10.1182/blood-2018-03-836932.
Full textHewitt, Kyle, Kirby D. Johnson, Duk-Hyoung Kim, Prithvia Devadas, Rajalekshmi Prathibha, Chandler Zuo, Colin Dewey, et al. "Cistrome Control of Hematopoieitic Stem/Progenitor Cell Function." Blood 126, no. 23 (December 3, 2015): 43. http://dx.doi.org/10.1182/blood.v126.23.43.43.
Full textThurner, Lorenz, Maria Kemele, Natalie Fadle, Evi Regitz, Patrick Roth, Michael Weller, Monika Szczepanowski, et al. "Postranslationally Modified Proteins in the Central Nervous System (CNS) Are the Dominant Antigenic Target/Stimulus of the B-Cell Receptor (BCR) in Primary CNS Lymphomas (PCNSL) Providing Strong Evidence for the Role of Chronic Autoantigenic Stimulation As an Early Step in the Pathogenesis of Aggressive B-Cell Lymphomas." Blood 124, no. 21 (December 6, 2014): 142. http://dx.doi.org/10.1182/blood.v124.21.142.142.
Full textTeng, Linda K. H., Brooke A. Pereira, Shivakumar Keerthikumar, Cheng Huang, Birunthi Niranjan, Sophie N. Lee, Michelle Richards, et al. "Mast Cell-Derived SAMD14 Is a Novel Regulator of the Human Prostate Tumor Microenvironment." Cancers 13, no. 6 (March 11, 2021): 1237. http://dx.doi.org/10.3390/cancers13061237.
Full textHewitt, Kyle, Prithvia Devadas, Lily Zemelko, Sunduz Keles, and Emery Bresnick. "SAMD14 enhancer-mediated hematopoietic stress signaling." Experimental Hematology 44, no. 9 (September 2016): S79. http://dx.doi.org/10.1016/j.exphem.2016.06.156.
Full textThurner, L., M. Bewarder, N. Fadle, E. Regitz, V. Poeschel, M. Ziepert, R. Schuck, et al. "SAMD14/NEURABIN-I AS BCR-ANTIGENS OF PRIMARY CENTRAL NERVOUS SYSTEM LYMPHOMA." Hematological Oncology 37 (June 2019): 195–96. http://dx.doi.org/10.1002/hon.9_2630.
Full textDissertations / Theses on the topic "SAMD14"
Sébert, Marie. "Génétique et évolution clonale des syndromes d’insuffisance médullaire." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC271.
Full textInherited bone marrow failure (IBMF) syndromes are heterogeneous diseases related to germ line mutations causing deficient hematopoiesis in mutated patients. Mutations involve several families of genes with different biological pathways driving the bone marrow failure. Most germ line genetic BMF disorders are characterized by a high propensity to clonal evolution and to develop MDS or AML. We used a whole-exome sequencing (WES) comprehensive analysis on fibroblast DNA samples from 179 patients with BMF/MDS of unresolved inherited origin. We provided a molecular diagnosis for 86/179 BMF patients (48%) including several seldom-reported IBMF/MDS entities like SAMD9/SAMD9L, MECOM/EVI1, and ERCC6L2. In particular, we described a specific clonal evolution in patients having mutations in SAMD9 and SAMD9L.Fanconi anemia (FA) is the most common IBMF syndrome, caused by a germ line mutation in one gene of the FA pathway. DNA repair deficiency in patient’s FA cells leads to chromosomal instability, which sets the stage for clonal evolution with a specific pattern of chromosomal abnormalities. We used integrated clinical, next-generation genomic and functional studies on primary cells from a National cohort of 335 FA patients, including 98 with clonal evolution, to decipher the mechanisms of BM progression. While relatively few somatic point mutations were found, unbalanced translocations leading to gross chromosomal copy-number abnormalities were most prominent. Whole genome sequencing revealed an FA-specific signature in which microhomology-mediated end joining (MMEJ) or non homologous end joining (NHEJ) repair had mediated genome rearrangements, consistent with the constitutive homologous repair defect. Longitudinal studies confirmed the order of chromosomal events during FA patients oncogenesis: 1q+, 3q+, -7/del7q, del or RUNX1 mutations. A major initial step was duplication of chromosome 1q, resulting in strong expression of MDM4, a negative regulator of p53, which can be targeted by MDM4-inhibitors.IBMF are rare diseases and our study participated to describe new genetic and clinical entities. Studying the clonal evolution of IBMF syndromes can help to understand MDS and AML pathophysiology and lead to therapeutic target identification
Hani, Lylia. "Caractérisation et rôle des lymphocytes T CD4+ mémoires SAMHD1low au cours de l'infection par le VIH-1." Thesis, Paris Est, 2018. http://www.theses.fr/2018PESC0087/document.
Full textWe have previously reported the presence of memory CD4+ T cells that display low levels of SAMHD1 (SAMHD1low ) enriched in Th17 and Tfh cells. Here we investigated gene expression profile and the size and composition of HIV DNA population in SAMHD1 low cells.A total of 36 individuals on c-ART (median: 7y) with median CD4+ counts and nadir of 549 cells/ul and 210 cells/ul respectively, including 6 elite controllers (EC, CD4+: 900 cells/ul) and 8 healthy donors were studied. Blood memory CD4+ CD45RO+ SAMHD1low, CD45RO+ SAMHD1high and naive CD45RO- SAMHD1high cells were sorted. Cell associated HIV-1 DNA levels were quantified (HIV DNA Cell, Biocentric) and ultra-deep-sequencing (UDS, 454/Roche) of partial env (C2/V3) HIV-1 DNA was performed. Gene expression profile on sorted cells was deternined with RNA-Sequencing (Illumina RNASeq technology). Levels of HIV-1 DNA were significantly higher in memory SAMHD1low cells compared to SAMHD1high cells (4.5 [3.1-6.2] vs 3.8 [2.9-5.7] log/10 6 cells, respectively, p=0.02) among c-ART individuals, while naïve CD45RO- SAMHD1high showed lower levels (3.1 [1.6-4.4]). EC exhibited low HIV-1 DNA level in both SAMHD1low and SAMHD1high (1.6 and 2.3 log/10 6 cells respectively p>0.05). Naïve CD45RO - SAMHD1 high cells from EC showed lower DNA compared to naïve cells from c-ART pts (1.6 and 3.1 log/10 6 cells, respectively, p=0.01). Phylogenetic analyses revealed well-segregated HIV-DNA populations between subsets with significant compartmentalization between SAMHD1low and SAMHD1high cells in all but 2 participants (p<0.001) and limited viral exchange. Moreover SAMHD1low cells exhibited a distinct gene profile as compared to SAMHD1high allowing thus further characterisation of these cells.This pilot study revealed distinct HIV DNA populations in size and composition associated with unique genes profile in memory SAMHD1low cells. We show that memory SAMHD1low cells exhibit distinct genes profile which segregates them from the SAMHD1 high counterpart, and contain the highest level of HIV-1 DNA. We reveal distinct/well-segregated HIV-1 DNA populations in both subsets, suggesting minimal viral exchange
Argüelles, Camilla. "Étude du rôle de la protéine de liaison aux ARN messagers Smaug dans la voie Hedgehog chez la drosophile." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC053.
Full textHedgehog Proteins (HH) are major players of animal development and carcinogenesis. Their transduction requires the 7 transmembrane protein Smoothened (SMO) whose activity is regulated by Patched (PTC), the HH receptor and antagonist. PTC and HH regulates SMO trafficking, phosphorylation and accumulation but numerous aspects of these regulations remain poorly understood. During my thesis, I focused on Smaug, a new partner of SMO in drosophila which was identified in the laboratory in a yeast two-hybrid screen. Smaug is known to bind and repress numerous mRNA during embryonic development in fly. I analyzed how it acts on SMO and HH signaling and also how is it regulated by HH. I have shown that Smaug is a positive regulator of the HH pathway and that it probably acts via its capacity to bind mRNA. I have also demonstrated that SMO and Smaug colocalise in cytoplasmic foci in absence of signal and that SMO is sufficient to localized Smaug to the plasma membrane in response to HH. Finally, I highlighted an effect of SMO and HH on the phosphorylation of Smaug suggesting the existence of a regulatory loop
Valverde, Estrella Lorena. "TREX1 and SAMHD1, and Aicardi-Goutières Syndrome." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/291940.
Full textLa síndrome d'Aicardi-Goutières (AGS), és una malaltia autoimmunitària recessiva que mimetitza una infecció vírica intrauterina, i la qual és caracteritzada per calcificacions intracranials, atròfia cerebral i augment d'IFN-alfa al líquid cefaloraquidi. L'AGS és una malaltia genètica heterogènia associada amb mutacions al gen que codifica per a l'exonucleasa TREX1, a qualsevol dels gens codificants per a les components de la ribonucleasa RNASE H2, a la fosfohidrolasa SAMHD1, a la deaminasa ADAR1 o al sensor citoplasmàtic MDA5. El coneixement d'aquestes funcions és fonamental per tal d'entendre la patogènesi de l'AGS. En aquesta tesi s'ha aprofundit en el coneixement del mecanisme regulador de la transcripció de Samhd1. Hem vist que Samhd1 es troba expressat en diferents òrgans sense necessitat de cap estímul previ, com el pàncrees, l’intestí prim i els macròfags derivats de moll d’os, i en diferents quantitats en altres òrgans de ratolí. Donada la important afectació que té l’AGS al cervell, també es va analitzar la seva expressió en neurones i cèl·lules de la micròglia. També hem vist que Samhd1 es troba induït en presència de citocines proinflamatòries, però no es troba afectada la seva expressió en presència de citocines antiinflamatòries així com tampoc en presència de TNF-gamma. Utilitzant macròfags derivats de ratolins deficients en STAT1, hem pogut demostrar que l’expressió de Samhd1 per IFN-alfa és a través d’STAT1, ja que la seva expressió es troba completament reprimida en aquestes cèl·lules. Ens vam centrar en la inducció de Samhd1 i per la seva comprensió vam focalitzar en l’estudi del seu promotor. Es van clonar 1500 parells de bases del promotor de Samhd1 en un plasmidi reporter de luciferasa, i es va veure que aquest fragment era suficient per induir l’expressió de luciferasa. A partir d’aquest constructe, es van realitzar llavors noves construccions delecionant cada vegada una regió del promotor. Es va veure que en delecionar una regió específica de 161pb, l’expressió de luciferasa es trobava completament reprimida, indicant que aquesta regió del promotor és crítica per a la inducció de Samhd1. Experiments de retard en gel (EMSA) van mostrar que Samhd1 es troba reprimit en condicions basals per una proteïna que no hem arribat a caracteritzar, i experiments de precipitació de cromatina (ChIP) van mostrar que IRF1 es troba involucrada en la inducció de Samhd1 per IFN-alfa. La nostra hipòtesi doncs, és que l’expressió de Samhd1 té un mecanisme de regulació doble: en condicions basals es troba reprimit i en presència d’IFN-alfa s’indueix una via de senyalització independent d’STAT1 que fa saltar el complex repressor del promotor, i també s’indueix una via de senyalització dependent d’STAT1, que indueix l’expressió d’IRF1 i que activa la transducció de Samhd1. Fins ara no hem caracteritzat la proteïna o complex de proteïnes que reprimeix l’expressió de Samhd1 en condicions basals, però s’està investigant mitjançant anàlisis proteòmics. En aquesta tesi també s’ha fet la construcció d’un ratolí KO condicional per a TREX1. Una vegada aconseguit aquest animal condicional, el qual conté el gen de Trex1 flanquejat per dues dianes LoxP, aquest s’està encreuant amb diferents soques que expressen CRE sota regulació de diferents Socs2 promotors. Els ratolins homozigots KO i que expressen CRE, tenen un fenotip similar al fenotip que mostren els ratolins KO totals de TREX1. Estem en el procés d’obtenció de ratolins homozigots KO i que expressen CRELysM però, donat a problemes amb la penetrància d’aquest al·lel, hem tingut algunes dificultats. Els resultats d’aquesta tesi en conjunt poden ajudar a entendre una mica més el funcionament de l'AGS.
Antonucci, Jenna Marie. "Mechanisms of HIV-1 Restriction by the Host Protein SAMHD1." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1524006072232491.
Full textLouis, Tania. "Étude des fonctions cellulaires de SAMHD1, facteur de restriction du VIH-1." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTS050/document.
Full textUnderstanding host pathogen interactions reveals not only important information regarding the replication cycle of the pathogen but it often leads to the discovery and better understanding of key biological processes of the host. The aim of my PhD was to decipher the cellular functions of the HIV-1 restriction factor SAMHD1. SAMHD1 (SAM domain and HD domain-containing protein 1) is expressed in most human tissues. This protein is able to hydrolyze cellular deoxyribonucleotides triphosphate (dNTP) and possesses a nuclease activity primarily against single stranded RNA. Mutations in SAMHD1 have been described in patients suffering from an auto-immune disease causing premature death of newborns. This phenotype suggests a role of SAMHD1 in the control of immune response. Moreover, SAMHD1 restricts HIV-1 in non-cycling cells. The HIV-2 accessory protein Vpx induces SAMHD1 degradation by the proteasome, conferring cell permissiveness to HIV. In fact, the antiviral activity of SAMHD1 has been extended to other viruses including Herpes Simplex Virus 1 and Hepatitis B virus. Nevertheless, the mechanism by which SAMHD1 restrict HIV replication is debated. It was initially thought to act by depleting the dNTP pool but recent studies highlighted a potential role of SAMHD1 nuclease function in degrading HIV-1 genomic RNA. Many studies aiming at understanding the antiviral activity of SAMHD1 are being pursued, whereas little is known about the cellular function of this protein. The fact that SAMHD1 is able to regulate the cellular dNTP pool and to interact with nucleic acids suggests a key role of this protein in cellular processes, such as DNA replication and repair. During my PhD, I showed that SAMHD1 modulates the cell cycle, as the overexpression of this protein slows down cell proliferation. I also observed that SAMHD1 overexpression increases cellular sensitivity to double strand DNA breaks-inducing agents. Moreover I discovered that, after double strand breaks induction, SAMHD1 is specifically regulated by phosphorylation on its threonine 592 and recruited at the damaged sites. Other studies confirmed the importance of SAMHD1 regulation along the cell cycle as its overexpression and depletion both decrease cell proliferation. In addition to my observations, some studies suggested that SAMHD1 is important to maintain genomic integrity, presumably through its implication in DNA repair. Altogether, these results promote SAMHD1 as a key player in cellular homeostasis. I additionally showed that SAMHD1 expression is reduced in 80% of patients suffering from chronic lymphocytic leukemia (CLL). SAMHD1 loss is therefore correlated to the development of a disease due to disturbances of cellular integrity. Looking at samples from different types of tumors, I showed that SAMHD1 loss is shared between all tested cancers, although at lesser extent than in CLL. My PhD work underlines the central role of SAMHD1 to maintain cellular integrity
Jaffer, Ali Mohammed Hakim. "Multifaceted roles of the transmembrane nuclear envelope protein, Samp1." Doctoral thesis, Stockholms universitet, Institutionen för neurokemi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-141816.
Full textAt the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript. Paper 5: Manuscript.
Silva, Maria-João. "Role of CTF18 and SAMHD1 in human DNA replication and genome integrity maintenance." Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20236.
Full textS phase is a critical period of the cell cycle during which the genome is particularly vulnerable. The efficient duplication of eukaryotic genomes depends on the unperturbed progression of thousands of replication forks.The early stages of tumorigenesis are associated with spontaneous replication stress, characterized with a blockage of fork progression. Understanding how replication stress arises in normal cells and contributes to tumorigenesis is a major challenge in cancer research.My thesis work aims at understanding the regulation of replication fork progression by two different proteins, SAMHD1 and CTF18, which have important roles in various aspects of DNA metabolism.Faithful duplication of the genome depends on a balanced supply of deoxyribonucleoside triphosphates (dNTPs). Imbalanced dNTP pools decrease the fidelity of DNA polymerases and increase mutation rates. SAMHD1 was originally identified as a dNTP triphosphohydrolase. This enzyme is implicated in Aicardi-Goutières syndrome. It has also been identified as a component of the human innate immune system that restricts HIV-1 infection. Recently, SAMHD1 was shown to be involved in the regulation of dNTP pools in cultured human cells. This protein is maximally expressed during quiescence and minimally during S phase. However, the impact of SAMHD1 upon DNA replication has not been addressed. Using DNA fiber spreading, we found that SAMHD1 modulates the speed of fork progression. In addition to its dNTPase activity, SAMHD1 contains a putative 3'-5' exonuclease domain that cleaves both DNA and RNA in vitro. A growing body of evidence indicates that 3'-5' exonucleases are critical to ensure fork progression and the fidelity of DNA replication. Remarkably, we found that the exonuclease activity of SAMHD1 promotes backtracking at paused forks and is important for replication fork progression. We propose that this backtracking activity is important to remove miss-incorporated deoxynucleotides or ribonucleotides. Our finding may have implications for our understanding of the link between SAMHD1 and the Aicardi-Goutières syndrome.CTF18 is part of a RFC-like complex involved in sister chromatid cohesion (SCC). In human cells it has been suggested that CTF18 controls the progression of replication forks, presumably by promoting acetylation of the SMC3 cohesin at replication forks. However, several results indicate that the function of CTF18 is not restricted to the establishment of SCC. Indeed, our group has shown that the yeast Ctf18 is essential for activation of the replication checkpoint, independently of its role in SCC. In human, CTF18 also participates in the recruitment of PCNA, the processivity factor of DNA polymerases δ and ε. CTF18 also interacts with the translesion polymerase . The aim of my work was to characterize the role of CTF18 during DNA replication. Using DNA combing, we first noticed that replication fork speed is slower in CTF18-depleted cells under unperturbed conditions. Intriguingly, increased fork speed was observed in CTF18-depleted cells challenged with hydroxyurea (HU), which is reminiscent of the phenotype of SAMHD1-depleted cells. Using iPOND, we observed an accumulation of PCNA at replication forks in HU-treated CTF18-depleted cells. We also found that CTF18 depletion induces an accumulation of yH2AX, suggesting that CTF18 is required for genome stability. Finally, we observed that the resection mediated by SAMHD1 at paused forks does not occur in the absence of CTF18. Together, these data indicate that CTF18 acts upstream of SAMHD1 at stalled forks, presumably through the unloading of PCNA
Qin, Zhihua. "SAMHD1 Negatively Regulates the Innate Immune Responses to Inflammatory Stimuli and Viral Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1587587968104986.
Full textCenker, Jennifer Jean. "DIFFERENTIAL HIV-1 SUSCEPTIBILITY OF PRIMARY MACROPHAGE POPULATIONS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1491656059069304.
Full textBooks on the topic "SAMD14"
Yŏm, Sang-sŏp. Samdae. Sŏul Tʻŭkpyŏlsi: Yangudang, 1986.
Find full text1948-, Kwŏn Yŏng-min, ed. Samdae. Sŏul: Minŭmsa, 1987.
Find full textSamdae. Sŏul-si: Chisŏng ŭi saem, 1991.
Find full textYŏm, Sang-sŏp. Samdae [oe]. Sŏul: Hagwŏn Chʻulpʻan Kongsa, 1987.
Find full textChʻoe, Chin-u. Pak Ssi samdae. Sŏul: Sosŏl Munhaksa, 1985.
Find full textCambodian Buddhist Temple (Washington, D.C.), ed. Braḥrājajīvapravatti nai Samdec Braḥsaṅgharāj Samdec Braḥsaṅghanāyak niṅ braḥmahāthera: Caek knuṅ okās buny Divā Samdec Juan Nāt. Kruṅ Vāsiṅtan, Dī. Sī: Vatt Buddhikārām, 1987.
Find full textLuvsanzunduĭ, S. Túúkhénd mónkhórsón Samdan avarga. Ulaanbaatar: Zhikom press, 2006.
Find full textSamdae: Yi Wŏn-ho changp'yŏn sosŏl. Sŏul T'ŭkpyŏlsi: P'aendŏm, 2010.
Find full textYŏm, Sang-sŏp. Samdae ; Manse chŏn ; Pʻyobonsil ŭi chʻŏng kaeguri [oe]. Sŏul: Tongsŏ Munhwasa, 1987.
Find full textYŏm Sang-sŏp "Samdae" ŭi inmul sŭt'orit'elling chŏllyak. Sŏul T'ŭkpyŏlsi: Munhyŏn, 2015.
Find full textBook chapters on the topic "SAMD14"
Kania, Stefan. "Samba4 als Printserver." In Samba 4, 379–96. München: Carl Hanser Verlag GmbH & Co. KG, 2019. http://dx.doi.org/10.3139/9783446457355.019.
Full textKania, Stefan. "WINS und Samba4." In Samba 4, 397–403. München: Carl Hanser Verlag GmbH & Co. KG, 2019. http://dx.doi.org/10.3139/9783446457355.020.
Full textde Silva, Suresh, Corine St. Gelais, Nagaraja Tirumuru, and Li Wu. "Counteraction of SAMHD1 by Vpx." In Encyclopedia of AIDS, 1–11. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-9610-6_375-1.
Full textde Silva, Suresh, Corine St. Gelais, Nagaraja Tirumuru, and Li Wu. "Counteraction of SAMHD1 by Vpx." In Encyclopedia of AIDS, 385–94. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_375.
Full textKania, Stefan. "Samba4 über die Kommandozeile verwalten." In Samba 4, 335–62. München: Carl Hanser Verlag GmbH & Co. KG, 2019. http://dx.doi.org/10.3139/9783446457355.017.
Full textChabah, Myriam, Nicolas Burlet, Jean-Philippe Malkasse, Guy Le Bihan, and Bruno Quellec. "SAMDIS: A New SAS Imaging System for AUV." In Quantitative Monitoring of the Underwater Environment, 107–18. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32107-3_10.
Full textKhaslan, Zaki, Noor Hidayah Mohd Yunus, Mohd Shahrul Mohd Nadzir, Jahariah Sampe, Noorazlina Mohamad Salih, and Kemal Maulana Alhasa. "IoT-Based Indoor Air Quality Monitoring System Using SAMD21 ARM Cortex Processor." In Advanced Structured Materials, 245–53. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92964-0_24.
Full textMaehigashi, Tatsuya, Dong-Hyun Kim, Raymond F. Schinazi, and Baek Kim. "SAMHD1-Mediated Negative Regulation of Cellular dNTP Levels: HIV-1, Innate Immunity, and Cancers." In Enzymatic and Chemical Synthesis of Nucleic Acid Derivatives, 313–25. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2018. http://dx.doi.org/10.1002/9783527812103.ch12.
Full textHolder, Andrew J., and Earl M. Evleth. "SAM1: General Description and Performance Evaluation for Hydrogen Bonds." In ACS Symposium Series, 113–24. Washington, DC: American Chemical Society, 1994. http://dx.doi.org/10.1021/bk-1994-0569.ch007.
Full textDong, Guozhong, Bo Wang, Wu Yang, Wei Wang, and Rui Sun. "SAMD: A System for Abnormal Messages Detection Oriented Microblog Message Stream." In Communications in Computer and Information Science, 113–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-49014-3_11.
Full textConference papers on the topic "SAMD14"
Bryant, Victoria, Jasmine Wong, Jason Schwartz, Tamara Lamprecht, Jing Ma, Charles Mullighan, Mignon Loh, Kevin Shannon, and Jeffery Klco. "Abstract 2063:SAMD9/SAMD9Lmutations in familial monosomy 7." 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.am2018-2063.
Full textMargeli, Mireia, Eudald Felip, Lucia Gutierrez Chamorro, Eva Riveira, Laura Layos, Teresa Moran, Margarita Romeo, Anna Matinez-Cardús, and Ester Ballana. "Abstract LB112: SAMHD1: A new Prognostic Marker in Breast Cancer (BC)." 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-lb112.
Full textSendon, C., Y. A. Collado, and A. E. Esquibies. "De Novo Variant of the SAMD9 Gene: Mirage Syndrome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5025.
Full textSakai, Michiya, Kenji Kanazawa, and Yasuki Ohtori. "Development of High Acceleration Shaking Table System Using Resonance Vibration." In ASME 2016 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/pvp2016-63752.
Full textFaraj, R., G. T. Kelly, A. Feng, and T. Wang. "A Novel Role of SAMD4A in Endothelial Cell Barrier Regulation in Response to Simvastatin." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5391.
Full textMargeli, Mireia, Eudald Felip, Maica Gomez, Pedro Fernandez, Laia Pérez-Roca, Eva Riveira-Muñoz, Anna Martinez-Cardús, et al. "Abstract P3-08-32: Predictive value of SAMHD1 expression in early relapse 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-p3-08-32.
Full textLee, Jaehun, Hochul Lee, Byoungjun Seo, Min Kyung Chae, Young Choon Lee, Hyuck Han, and Sooyong Kang. "SAMD Apps: Install Once, Run Anywhere Instantly." In 2018 IEEE International Conference on Pervasive Computing and Communications Workshops (PerCom Workshops). IEEE, 2018. http://dx.doi.org/10.1109/percomw.2018.8480287.
Full textFelip, Eudald, Roger Badia, Mireia Margelí, Marc Castellví, Vanesa Quiroga, Iris Teruel, Beatriz Cirauqui, et al. "Abstract P5-05-14: Cyclin-dependent kinases inhibitors improve antimetabolite drug potency depending on SAMHD1 expression." 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-p5-05-14.
Full textLee, Jaehun, Hochul Lee, Byoungjun Seo, Young Choon Lee, Hyuck Han, and Sooyong Kang. "SAMD: Fine-Grained Application Sharing for Mobile Collaboration." In 2018 IEEE International Conference on Pervasive Computing and Communications (PerCom). IEEE, 2018. http://dx.doi.org/10.1109/percom.2018.8444574.
Full textSchwartz, Jason R., Jon P. Connelly, Shondra M. Pruett-Miller, and Jeffery M. Klco. "Abstract B49: Modeling a pathogenic SAMD9 mutation in human induced pluripotent stem cells." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-b49.
Full textReports on the topic "SAMD14"
Holder, Andrew J. SAM1-A New Semiempirical Method Including D-Orbitals. Fort Belvoir, VA: Defense Technical Information Center, January 1995. http://dx.doi.org/10.21236/ada290903.
Full textManni, Andrea. Relative Contribution of Ornithine Decarboxylase (ODC) Versus S-adenosylmethionine Decarboxylase (SAMDC) to Human Breast Cancer Progression and Development. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408110.
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