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Article ; Online: DLL3 regulates Notch signaling in small cell lung cancer.

Kim, Jun W / Ko, Julie H / Sage, Julien

iScience

2022 Volume 25, Issue 12, Page(s) 105603

Abstract: Tumor heterogeneity plays a critical role in tumor development and response to treatment. In small-cell lung cancer (SCLC), intratumoral heterogeneity is driven in part by the Notch signaling pathway, which reprograms neuroendocrine cancer cells to a ... ...

Abstract	Tumor heterogeneity plays a critical role in tumor development and response to treatment. In small-cell lung cancer (SCLC), intratumoral heterogeneity is driven in part by the Notch signaling pathway, which reprograms neuroendocrine cancer cells to a less/non-neuroendocrine state. Here we investigated the atypical Notch ligand DLL3 as a biomarker of the neuroendocrine state and a regulator of cell-cell interactions in SCLC. We first built a mathematical model to predict the impact of DLL3 expression on SCLC cell populations. We next tested this model using a single-chain variable fragment (scFv) to track DLL3 expression
Language	English
Publishing date	2022-11-16
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.105603
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Article ; Online: Mechanisms of small cell lung cancer metastasis.

Ko, Julie / Winslow, Monte M / Sage, Julien

EMBO molecular medicine

2020 Volume 13, Issue 1, Page(s) e13122

Abstract: Metastasis is a major cause of morbidity and mortality in cancer patients. However, the molecular and cellular mechanisms underlying the ability of cancer cells to metastasize remain relatively poorly understood. Among all solid tumors, small cell lung ... ...

Abstract	Metastasis is a major cause of morbidity and mortality in cancer patients. However, the molecular and cellular mechanisms underlying the ability of cancer cells to metastasize remain relatively poorly understood. Among all solid tumors, small cell lung cancer (SCLC) has remarkable metastatic proclivity, with a majority of patients diagnosed with metastatic disease. Our understanding of SCLC metastasis has been hampered for many years by the paucity of material from primary tumors and metastases, as well as the lack of faithful pre-clinical models. Here, we review recent advances that are helping circumvent these limitations. These advances include methods that employ circulating tumor cells from the blood of SCLC patients and the development of diverse genetically engineered mouse models of metastatic SCLC. New insights into the cellular mechanisms of SCLC metastasis include observations of cell fate changes associated with increased metastatic ability. Ongoing studies on cell migration and organ tropism promise to expand our understanding of SCLC metastasis. Ultimately, a better molecular understanding of metastatic phenotypes may be translated into new therapeutic options to limit metastatic spread and treat metastatic SCLC.
MeSH term(s)	Animals ; Cell Movement ; Humans ; Lung Neoplasms ; Mice ; Neoplasm Metastasis ; Small Cell Lung Carcinoma
Language	English
Publishing date	2020-12-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202013122
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Article ; Online: Small Cell Lung Cancer Plasticity Enables NFIB-Independent Metastasis.

Ko, Julie H / Lambert, Kyle E / Bhattacharya, Debadrita / Lee, Myung Chang / Colón, Caterina I / Hauser, Haley / Sage, Julien

Cancer research

2023 Volume 84, Issue 2, Page(s) 226–240

Abstract: Metastasis is a major cause of morbidity and mortality in patients with cancer, highlighting the need to identify improved treatment and prevention strategies. Previous observations in preclinical models and tumors from patients with small cell lung ... ...

Abstract	Metastasis is a major cause of morbidity and mortality in patients with cancer, highlighting the need to identify improved treatment and prevention strategies. Previous observations in preclinical models and tumors from patients with small cell lung cancer (SCLC), a fatal form of lung cancer with high metastatic potential, identified the transcription factor NFIB as a driver of tumor growth and metastasis. However, investigation into the requirement for NFIB activity for tumor growth and metastasis in relevant in vivo models is needed to establish NFIB as a therapeutic target. Here, using conditional gene knockout strategies in genetically engineered mouse models of SCLC, we found that upregulation of NFIB contributes to tumor progression, but NFIB is not required for metastasis. Molecular studies in NFIB wild-type and knockout tumors identified the pioneer transcription factors FOXA1/2 as candidate drivers of metastatic progression. Thus, while NFIB upregulation is a frequent event in SCLC during tumor progression, SCLC tumors can employ NFIB-independent mechanisms for metastasis, further highlighting the plasticity of these tumors. Significance: Small cell lung cancer cells overcome deficiency of the prometastatic oncogene NFIB to gain metastatic potential through various molecular mechanisms, which may represent targets to block progression of this fatal cancer type.
MeSH term(s)	Animals ; Humans ; Mice ; Lung Neoplasms/pathology ; NFI Transcription Factors/genetics ; NFI Transcription Factors/metabolism ; Oncogenes ; Small Cell Lung Carcinoma/pathology
Chemical Substances	NFI Transcription Factors ; NFIB protein, human
Language	English
Publishing date	2023-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-23-1079
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Article ; Online: An age-related change in the ipsilateral silent period of a small hand muscle.

Petitjean, Michel / Ko, Julie Yeung Lam

Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology

2013 Volume 124, Issue 2, Page(s) 346–353

Abstract: Objective: To establish the presence or absence of an age effect on the ipsilateral silent period (iSP) for the abductor pollicis brevis (APB) muscle in healthy subjects.: Methods: Twenty young adults (10 men, 10 women; age range: 20-40) and 20 older ...

Abstract	Objective: To establish the presence or absence of an age effect on the ipsilateral silent period (iSP) for the abductor pollicis brevis (APB) muscle in healthy subjects. Methods: Twenty young adults (10 men, 10 women; age range: 20-40) and 20 older adults (10 men, 10 women; age range: 50-70) were matched by age (+30 years), gender and height (±5 cm). All were right-handed. We investigated the iSP for the APB by applying transcranial magnetic stimulation (TMS) and recording surface electromyograms. The contralateral motor-evoked potential (MEP) onset latency, the iSP onset and end latency (iSPOL and iSPEL) were measured and the iSP duration (iSPD) and transcallosal conduction time (TCT) were calculated. We evaluated the correlation between age and iSP, the latter's intra- and intersession reproducibility and potential influencing factors. Results: Mean iSPOL, iSPEL and TCT values were significantly greater in older adults (both men and women) than in young adults. Intra- and intersession reproducibility was good. The mean left-side iSPEL and iSPD were longer than the right-side mean values in young adults but not in older adults. In both age groups, women displayed shorter latencies than men. Conclusions: There is a strong effect of age on iSP parameters. Significance: Our iSP results may evidence a decrease in transcallosal excitability with age, rather than slowing of the transcallosal interneuron conduction velocity.
MeSH term(s)	Adult ; Aged ; Aging/physiology ; Electromyography ; Evoked Potentials, Motor/physiology ; Female ; Hand/innervation ; Hand/physiology ; Humans ; Male ; Middle Aged ; Motor Cortex/physiology ; Muscle, Skeletal/innervation ; Neural Conduction/physiology ; Reaction Time/physiology ; Time Factors ; Transcranial Magnetic Stimulation
Language	English
Publishing date	2013-02
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1463630-x
ISSN	1872-8952 ; 0921-884X ; 1388-2457
ISSN (online)	1872-8952
ISSN	0921-884X ; 1388-2457
DOI	10.1016/j.clinph.2012.07.006
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Article ; Online: A multiplexed in vivo approach to identify driver genes in small cell lung cancer.

Lee, Myung Chang / Cai, Hongchen / Murray, Christopher W / Li, Chuan / Shue, Yan Ting / Andrejka, Laura / He, Andy L / Holzem, Alessandra M E / Drainas, Alexandros P / Ko, Julie H / Coles, Garry L / Kong, Christina / Zhu, Shirley / Zhu, ChunFang / Wang, Jason / van de Rijn, Matt / Petrov, Dmitri A / Winslow, Monte M / Sage, Julien

Cell reports

2023 Volume 42, Issue 1, Page(s) 111990

Abstract: Small cell lung cancer (SCLC) is a lethal form of lung cancer. Here, we develop a quantitative multiplexed approach on the basis of lentiviral barcoding with somatic CRISPR-Cas9-mediated genome editing to functionally investigate candidate regulators of ... ...

Abstract	Small cell lung cancer (SCLC) is a lethal form of lung cancer. Here, we develop a quantitative multiplexed approach on the basis of lentiviral barcoding with somatic CRISPR-Cas9-mediated genome editing to functionally investigate candidate regulators of tumor initiation and growth in genetically engineered mouse models of SCLC. We found that naphthalene pre-treatment enhances lentiviral vector-mediated SCLC initiation, enabling high multiplicity of tumor clones for analysis through high-throughput sequencing methods. Candidate drivers of SCLC identified from a meta-analysis across multiple human SCLC genomic datasets were tested using this approach, which defines both positive and detrimental impacts of inactivating 40 genes across candidate pathways on SCLC development. This analysis and subsequent validation in human SCLC cells establish TSC1 in the PI3K-AKT-mTOR pathway as a robust tumor suppressor in SCLC. This approach should illuminate drivers of SCLC, facilitate the development of precision therapies for defined SCLC genotypes, and identify therapeutic targets.
MeSH term(s)	Mice ; Animals ; Humans ; Small Cell Lung Carcinoma/pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Lung Neoplasms/pathology ; Genes, Tumor Suppressor ; Genomics
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-01-13
Publishing country	United States
Document type	Meta-Analysis ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.111990
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Article ; Online: Single-chromosome Gains Commonly Function as Tumor Suppressors.

Sheltzer, Jason M / Ko, Julie H / Replogle, John M / Habibe Burgos, Nicole C / Chung, Erica S / Meehl, Colleen M / Sayles, Nicole M / Passerini, Verena / Storchova, Zuzana / Amon, Angelika

Cancer cell

2017 Volume 31, Issue 2, Page(s) 240–255

Abstract: Aneuploidy is a hallmark of cancer, although its effects on tumorigenesis are unclear. Here, we investigated the relationship between aneuploidy and cancer development using cells engineered to harbor single extra chromosomes. We found that nearly all ... ...

Abstract	Aneuploidy is a hallmark of cancer, although its effects on tumorigenesis are unclear. Here, we investigated the relationship between aneuploidy and cancer development using cells engineered to harbor single extra chromosomes. We found that nearly all trisomic cell lines grew poorly in vitro and as xenografts, relative to genetically matched euploid cells. Moreover, the activation of several oncogenic pathways failed to alleviate the fitness defect induced by aneuploidy. However, following prolonged growth, trisomic cells acquired additional chromosomal alterations that were largely absent from their euploid counterparts and that correlated with improved fitness. Thus, while single-chromosome gains can suppress transformation, the genome-destabilizing effects of aneuploidy confer an evolutionary flexibility that may contribute to the aggressive growth of advanced malignancies with complex karyotypes.
MeSH term(s)	Aneuploidy ; Animals ; Cell Proliferation ; Cell Transformation, Neoplastic ; Chromosome Aberrations ; Genes, ras ; Genomic Instability ; HCT116 Cells ; Humans ; Neoplasms/genetics ; Neoplasms/prevention & control ; Oncogenes
Language	English
Publishing date	2017-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2016.12.004
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Article ; Online: Unbiased Proteomic Profiling Uncovers a Targetable GNAS/PKA/PP2A Axis in Small Cell Lung Cancer Stem Cells.

Coles, Garry L / Cristea, Sandra / Webber, James T / Levin, Rebecca S / Moss, Steven M / He, Andy / Sangodkar, Jaya / Hwang, Yeonjoo C / Arand, Julia / Drainas, Alexandros P / Mooney, Nancie A / Demeter, Janos / Spradlin, Jessica N / Mauch, Brandon / Le, Vicky / Shue, Yan Ting / Ko, Julie H / Lee, Myung Chang / Kong, Christina /

Nomura, Daniel K / Ohlmeyer, Michael / Swaney, Danielle L / Krogan, Nevan J / Jackson, Peter K / Narla, Goutham / Gordan, John D / Shokat, Kevan M / Sage, Julien

Cancer cell

2020 Volume 38, Issue 1, Page(s) 129–143.e7

Abstract: Using unbiased kinase profiling, we identified protein kinase A (PKA) as an active kinase in small cell lung cancer (SCLC). Inhibition of PKA activity genetically, or pharmacologically by activation of the PP2A phosphatase, suppresses SCLC expansion in ... ...

Abstract	Using unbiased kinase profiling, we identified protein kinase A (PKA) as an active kinase in small cell lung cancer (SCLC). Inhibition of PKA activity genetically, or pharmacologically by activation of the PP2A phosphatase, suppresses SCLC expansion in culture and in vivo. Conversely, GNAS (G-protein α subunit), a PKA activator that is genetically activated in a small subset of human SCLC, promotes SCLC development. Phosphoproteomic analyses identified many PKA substrates and mechanisms of action. In particular, PKA activity is required for the propagation of SCLC stem cells in transplantation studies. Broad proteomic analysis of recalcitrant cancers has the potential to uncover targetable signaling networks, such as the GNAS/PKA/PP2A axis in SCLC.
MeSH term(s)	A549 Cells ; Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Chromogranins/genetics ; Chromogranins/metabolism ; Cisplatin/administration & dosage ; Cisplatin/pharmacology ; Cyclic AMP-Dependent Protein Kinases/genetics ; Cyclic AMP-Dependent Protein Kinases/metabolism ; GTP-Binding Protein alpha Subunits, Gs/genetics ; GTP-Binding Protein alpha Subunits, Gs/metabolism ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Neoplastic Stem Cells/metabolism ; Protein Phosphatase 2/genetics ; Protein Phosphatase 2/metabolism ; Proteomics/methods ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/genetics ; Small Cell Lung Carcinoma/metabolism ; Xenograft Model Antitumor Assays/methods
Chemical Substances	Antineoplastic Agents ; Chromogranins ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Protein Phosphatase 2 (EC 3.1.3.16) ; GNAS protein, human (EC 3.6.1.-) ; GTP-Binding Protein alpha Subunits, Gs (EC 3.6.5.1) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2020-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2020.05.003
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Article ; Online: Effect of transcranial magnetic stimulation on four types of pressure-programmable valves.

Lefranc, Michel / Ko, Julie Yeung Lam / Peltier, Johann / Fichten, Anthony / Desenclos, Christine / Macron, Jean-Michel / Toussaint, Patrick / Le Gars, Daniel / Petitjean, Michel

Acta neurochirurgica

2010 Volume 152, Issue 4, Page(s) 689–697

Abstract: Background: Exposure to powerful magnetic fields may alter the settings of programmable ventriculoperitoneal shunt valves or even cause permanent damage to these devices. Transcranial magnetic stimulation (TMS) and magnetic resonance imaging both ... ...

Abstract	Background: Exposure to powerful magnetic fields may alter the settings of programmable ventriculoperitoneal shunt valves or even cause permanent damage to these devices. Transcranial magnetic stimulation (TMS) and magnetic resonance imaging both generate a high-intensity, focal magnetic field. To the best of our knowledge, there is no literature data on the compatibility of TMS with neurosurgical implants. The aim of the present in vitro study was to investigate the effects of TMS on four types of pressure-programmable valves (the Strata 2 from Medtronic, the Polaris from Sophysa, the ProGAV from Miethke, and a cylindrical valve from Codman-Hakim). Methods: We used a Magpro X100 stimulator (Medtronic) for monophasic or biphasic TMS via a circular or a figure-of-eight coil. Each valve setting was tested before and after exposure to TMS. Experiment 1: The effect of the coil-valve distance (10, 5, 2.5, and 1 cm) was assessed. Experiment 2: We mimicked in situ stimulation with a human mannequin by placing the valve in a retroauricular position, the TMS circular coil on the apex, and figure-of-eight coil centered over the primary motor area site. Temperature changes were monitored throughout the experiments. Experience 3: TMS-induced valve movements were assessed by using an in-house accelerometric setup. Results: Our results primarily demonstrated that the Strata 2 and Codman-Hakim valves' settings were perturbed by TMS. There was no heating effect for any of the valves. However, TMS induced movements of the Strata 2, Polaris, and ProGAV valves. Experiment 1: The unsetting frequencies observed for the Strata 2 and the Codman-Hakim valve showed an influence of the distance, the coil model, and the magnetic field characteristics, whereas the Polaris and ProGAV's settings remained unchanged. Experiment 2: Unsetting occurred for Strata 2 valve with the circular coil only, whereas the Polaris, ProGAV, and Codman-Hakim valves' settings remained stable. Experiment 3: The Strata 2, Polaris, and ProGAV valves showed high-amplitude oscillations during TMS under all stimulation conditions, whereas the Codman-Hakim valve did not move. Conclusions: Our in vitro experiments showed that TMS can interfere with programmable shunt valves by inducing unsetting or movement. This finding suggests that great care must be taken if applying TMS in hydrocephalic, shunted patients.
MeSH term(s)	Cerebrospinal Fluid Pressure/physiology ; Equipment Design ; Equipment Failure Analysis ; Humans ; Hydrocephalus/surgery ; In Vitro Techniques ; Models, Anatomic ; Software ; Therapy, Computer-Assisted/instrumentation ; Transcranial Magnetic Stimulation/adverse effects ; Transcranial Magnetic Stimulation/instrumentation ; Ventriculoperitoneal Shunt/instrumentation
Language	English
Publishing date	2010-04
Publishing country	Austria
Document type	Comparative Study ; Journal Article
ZDB-ID	80010-7
ISSN	0942-0940 ; 0001-6268
ISSN (online)	0942-0940
ISSN	0001-6268
DOI	10.1007/s00701-009-0564-2
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Article ; Online: A functional genomics screen identifying blood cell development genes in Drosophila by undergraduates participating in a course-based research experience.

Evans, Cory J / Olson, John M / Mondal, Bama Charan / Kandimalla, Pratyush / Abbasi, Ariano / Abdusamad, Mai M / Acosta, Osvaldo / Ainsworth, Julia A / Akram, Haris M / Albert, Ralph B / Alegria-Leal, Elitzander / Alexander, Kai Y / Ayala, Angelica C / Balashova, Nataliya S / Barber, Rebecca M / Bassi, Harmanjit / Bennion, Sean P / Beyder, Miriam / Bhatt, Kush V /

Bhoot, Chinmay / Bradshaw, Aaron W / Brannigan, Tierney G / Cao, Boyu / Cashell, Yancey Y / Chai, Timothy / Chan, Alex W / Chan, Carissa / Chang, Inho / Chang, Jonathan / Chang, Michael T / Chang, Patrick W / Chang, Stephen / Chari, Neel / Chassiakos, Alexander J / Chen, Iris E / Chen, Vivian K / Chen, Zheying / Cheng, Marsha R / Chiang, Mimi / Chiu, Vivian / Choi, Sharon / Chung, Jun Ho / Contreras, Liset / Corona, Edgar / Cruz, Courtney J / Cruz, Renae L / Dang, Jefferson M / Dasari, Suhas P / De La Fuente, Justin R O / Del Rio, Oscar M A / Dennis, Emily R / Dertsakyan, Petros S / Dey, Ipsita / Distler, Rachel S / Dong, Zhiqiao / Dorman, Leah C / Douglass, Mark A / Ehresman, Allysen B / Fu, Ivy H / Fua, Andrea / Full, Sean M / Ghaffari-Rafi, Arash / Ghani, Asmar Abdul / Giap, Bosco / Gill, Sonia / Gill, Zafar S / Gills, Nicholas J / Godavarthi, Sindhuja / Golnazarian, Talin / Goyal, Raghav / Gray, Ricardo / Grunfeld, Alexander M / Gu, Kelly M / Gutierrez, Natalia C / Ha, An N / Hamid, Iman / Hanson, Ashley / Hao, Celesti / He, Chongbin / He, Mengshi / Hedtke, Joshua P / Hernandez, Ysrael K / Hlaing, Hnin / Hobby, Faith A / Hoi, Karen / Hope, Ashley C / Hosseinian, Sahra M / Hsu, Alice / Hsueh, Jennifer / Hu, Eileen / Hu, Spencer S / Huang, Stephanie / Huang, Wilson / Huynh, Melanie / Javier, Carmen / Jeon, Na Eun / Ji, Sunjong / Johal, Jasmin / John, Amala / Johnson, Lauren / Kadakia, Saurin / Kakade, Namrata / Kamel, Sarah / Kaur, Ravinder / Khatra, Jagteshwar S / Kho, Jeffrey A / Kim, Caleb / Kim, Emily Jin-Kyung / Kim, Hee Jong / Kim, Hyun Wook / Kim, Jin Hee / Kim, Seong Ah / Kim, Woo Kyeom / Kit, Brian / La, Cindy / Lai, Jonathan / Lam, Vivian / Le, Nguyen Khoi / Lee, Chi Ju / Lee, Dana / Lee, Dong Yeon / Lee, James / Lee, Jason / Lee, Jessica / Lee, Ju-Yeon / Lee, Sharon / Lee, Terrence C / Lee, Victoria / Li, Amber J / Li, Jialing / Libro, Alexandra M / Lien, Irvin C / Lim, Mia / Lin, Jeffrey M / Liu, Connie Y / Liu, Steven C / Louie, Irene / Lu, Shijia W / Luo, William Y / Luu, Tiffany / Madrigal, Josef T / Mai, Yishan / Miya, Darron I / Mohammadi, Mina / Mohanta, Sayonika / Mokwena, Tebogo / Montoya, Tonatiuh / Mould, Dallas L / Murata, Mark R / Muthaiya, Janani / Naicker, Seethim / Neebe, Mallory R / Ngo, Amy / Ngo, Duy Q / Ngo, Jamie A / Nguyen, Anh T / Nguyen, Huy C X / Nguyen, Rina H / Nguyen, Thao T T / Nguyen, Vincent T / Nishida, Kevin / Oh, Seo-Kyung / Omi, Kristen M / Onglatco, Mary C / Almazan, Guadalupe Ortega / Paguntalan, Jahzeel / Panchal, Maharshi / Pang, Stephanie / Parikh, Harin B / Patel, Purvi D / Patel, Trisha H / Petersen, Julia E / Pham, Steven / Phan-Everson, Tien M / Pokhriyal, Megha / Popovich, Davis W / Quaal, Adam T / Querubin, Karl / Resendiz, Anabel / Riabkova, Nadezhda / Rong, Fred / Salarkia, Sarah / Sama, Nateli / Sang, Elaine / Sanville, David A / Schoen, Emily R / Shen, Zhouyang / Siangchin, Ken / Sibal, Gabrielle / Sin, Garuem / Sjarif, Jasmine / Smith, Christopher J / Soeboer, Annisa N / Sosa, Cristian / Spitters, Derek / Stender, Bryan / Su, Chloe C / Summapund, Jenny / Sun, Beatrice J / Sutanto, Christine / Tan, Jaime S / Tan, Nguon L / Tangmatitam, Parich / Trac, Cindy K / Tran, Conny / Tran, Daniel / Tran, Duy / Tran, Vina / Truong, Patrick A / Tsai, Brandon L / Tsai, Pei-Hua / Tsui, C Kimberly / Uriu, Jackson K / Venkatesh, Sanan / Vo, Maique / Vo, Nhat-Thi / Vo, Phuong / Voros, Timothy C / Wan, Yuan / Wang, Eric / Wang, Jeffrey / Wang, Michael K / Wang, Yuxuan / Wei, Siman / Wilson, Matthew N / Wong, Daniel / Wu, Elliott / Xing, Hanning / Xu, Jason P / Yaftaly, Sahar / Yan, Kimberly / Yang, Evan / Yang, Rebecca / Yao, Tony / Yeo, Patricia / Yip, Vivian / Yogi, Puja / Young, Gloria Chin / Yung, Maggie M / Zai, Alexander / Zhang, Christine / Zhang, Xiao X / Zhao, Zijun / Zhou, Raymond / Zhou, Ziqi / Abutouk, Mona / Aguirre, Brian / Ao, Chon / Baranoff, Alexis / Beniwal, Angad / Cai, Zijie / Chan, Ryan / Chien, Kenneth Chang / Chaudhary, Umar / Chin, Patrick / Chowdhury, Praptee / Dalie, Jamlah / Du, Eric Y / Estrada, Alec / Feng, Erwin / Ghaly, Monica / Graf, Rose / Hernandez, Eduardo / Herrera, Kevin / Ho, Vivien W / Honeychurch, Kaitlyn / Hou, Yurianna / Huang, Jo M / Ishii, Momoko / James, Nicholas / Jang, Gah-Eun / Jin, Daphne / Juarez, Jesse / Kesaf, Ayse Elif / Khalsa, Sat Kartar / Kim, Hannah / Kovsky, Jenna / Kuang, Chak Lon / Kumar, Shraddha / Lam, Gloria / Lee, Ceejay / Lee, Grace / Li, Li / Lin, Joshua / Liu, Josephine / Ly, Janice / Ma, Austin / Markovic, Hannah / Medina, Cristian / Mungcal, Jonelle / Naranbaatar, Bilguudei / Patel, Kayla / Petersen, Lauren / Phan, Amanda / Phung, Malcolm / Priasti, Nadiyah / Ruano, Nancy / Salim, Tanveer / Schnell, Kristen / Shah, Paras / Shen, Jinhua / Stutzman, Nathan / Sukhina, Alisa / Tian, Rayna / Vega-Loza, Andrea / Wang, Joyce / Wang, Jun / Watanabe, Rina / Wei, Brandon / Xie, Lillian / Ye, Jessica / Zhao, Jeffrey / Zimmerman, Jill / Bracken, Colton / Capili, Jason / Char, Andrew / Chen, Michel / Huang, Pingdi / Ji, Sena / Kim, Emily / Kim, Kenneth / Ko, Julie / Laput, Sean Louise G / Law, Sam / Lee, Sang Kuk / Lee, Olivia / Lim, David / Lin, Eric / Marik, Kyle / Mytych, Josh / O'Laughlin, Andie / Pak, Jensen / Park, Claire / Ryu, Ruth / Shinde, Ashwin / Sosa, Manny / Waite, Nick / Williams, Mane / Wong, Richard / Woo, Jocelyn / Woo, Jonathan / Yepuri, Vishaal / Yim, Dorothy / Huynh, Dan / Wijiewarnasurya, Dinali / Shapiro, Casey / Levis-Fitzgerald, Marc / Jaworski, Leslie / Lopatto, David / Clark, Ira E / Johnson, Tracy / Banerjee, Utpal

G3 (Bethesda, Md.)

2021 Volume 11, Issue 1

Abstract: Undergraduate students participating in the UCLA Undergraduate Research Consortium for Functional Genomics (URCFG) have conducted a two-phased screen using RNA interference (RNAi) in combination with fluorescent reporter proteins to identify genes ... ...

Abstract	Undergraduate students participating in the UCLA Undergraduate Research Consortium for Functional Genomics (URCFG) have conducted a two-phased screen using RNA interference (RNAi) in combination with fluorescent reporter proteins to identify genes important for hematopoiesis in Drosophila. This screen disrupted the function of approximately 3500 genes and identified 137 candidate genes for which loss of function leads to observable changes in the hematopoietic development. Targeting RNAi to maturing, progenitor, and regulatory cell types identified key subsets that either limit or promote blood cell maturation. Bioinformatic analysis reveals gene enrichment in several previously uncharacterized areas, including RNA processing and export and vesicular trafficking. Lastly, the participation of students in this course-based undergraduate research experience (CURE) correlated with increased learning gains across several areas, as well as increased STEM retention, indicating that authentic, student-driven research in the form of a CURE represents an impactful and enriching pedagogical approach.
MeSH term(s)	Animals ; Blood Cells ; Drosophila/genetics ; Genomics/education ; Humans ; Students ; Universities
Language	English
Publishing date	2021-02-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1093/g3journal/jkaa028
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Expression-Based Cell Lineage Analysis in

Olson, John M / Evans, Cory J / Ngo, Kathy T / Kim, Hee Jong / Nguyen, Joseph Duy / Gurley, Kayla G H / Ta, Truc / Patel, Vijay / Han, Lisa / Truong-N, Khoa T / Liang, Letty / Chu, Maggie K / Lam, Hiu / Ahn, Hannah G / Banerjee, Abhik Kumar / Choi, In Young / Kelley, Ross G / Moridzadeh, Naseem / Khan, Awais M /

Khan, Omair / Lee, Szuyao / Johnson, Elizabeth B / Tigranyan, Annie / Wang, Jay / Gandhi, Anand D / Padhiar, Manish M / Calvopina, Joseph Hargan / Sumra, Kirandeep / Ou, Kristy / Wu, Jessie C / Dickan, Joseph N / Ahmadi, Sabrena M / Allen, Donald N / Mai, Van Thanh / Ansari, Saif / Yeh, George / Yoon, Earl / Gon, Kimberly / Yu, John Y / He, Johnny / Zaretsky, Jesse M / Lee, Noemi E / Kuoy, Edward / Patananan, Alexander N / Sitz, Daniel / Tran, PhuongThao / Do, Minh-Tu / Akhave, Samira J / Alvarez, Silverio D / Asem, Bobby / Asem, Neda / Azarian, Nicole A / Babaesfahani, Arezou / Bahrami, Ahmad / Bhamra, Manjeet / Bhargava, Ragini / Bhatia, Rakesh / Bhatia, Subir / Bumacod, Nicholas / Caine, Jonathan J / Caldwell, Thomas A / Calica, Nicole A / Calonico, Elise M / Chan, Carman / Chan, Helen H-L / Chang, Albert / Chang, Chiaen / Chang, Daniel / Chang, Jennifer S / Charania, Nauman / Chen, Jasmine Y / Chen, Kevin / Chen, Lu / Chen, Yuyu / Cheung, Derek J / Cheung, Jesse J / Chew, Jessica J / Chew, Nicole B / Chien, Cheng-An Tony / Chin, Alana M / Chin, Chee Jia / Cho, Youngho / Chou, Man Ting / Chow, Ke-Huan K / Chu, Carolyn / Chu, Derrick M / Chu, Virginia / Chuang, Katherine / Chugh, Arunit Singh / Cubberly, Mark R / Daniel, Michael Guillermo / Datta, Sangita / Dhaliwal, Raj / Dinh, Jenny / Dixit, Dhaval / Dowling, Emmylou / Feng, Melinda / From, Christopher M / Furukawa, Daisuke / Gaddipati, Himaja / Gevorgyan, Lilit / Ghaznavi, Zunera / Ghosh, Tulika / Gill, Jaskaran / Groves, David J / Gurara, Kalkidan K / Haghighi, Ali R / Havard, Alexandra L / Heyrani, Nasser / Hioe, Tanya / Hong, Kirim / Houman, Justin J / Howland, Molly / Hsia, Elaine L / Hsueh, Justin / Hu, Stacy / Huang, Andrew J / Huynh, Jasmine C / Huynh, Jenny / Iwuchukwu, Chris / Jang, Michael J / Jiang, An An / Kahlon, Simran / Kao, Pei-Yun / Kaur, Manpreet / Keehn, Matthew G / Kim, Elizabeth J / Kim, Hannah / Kim, Michelle J / Kim, Shawn J / Kitich, Aleksandar / Kornberg, Ross A / Kouzelos, Nicholas G / Kuon, Jane / Lau, Bryan / Lau, Roger K / Law, Rona / Le, Huy D / Le, Rachael / Lee, Carrou / Lee, Christina / Lee, Grace E / Lee, Kenny / Lee, Michelle J / Lee, Regina V / Lee, Sean H K / Lee, Sung Kyu / Lee, Sung-Ling D / Lee, Yong Jun / Leong, Megan J / Li, David M / Li, Hao / Liang, Xingfu / Lin, Eric / Lin, Michelle M / Lin, Peter / Lin, Tiffany / Lu, Stacey / Luong, Serena S / Ma, Jessica S / Ma, Li / Maghen, Justin N / Mallam, Sravya / Mann, Shivtaj / Melehani, Jason H / Miller, Ryan C / Mittal, Nitish / Moazez, Carmel M / Moon, Susie / Moridzadeh, Rameen / Ngo, Kaley / Nguyen, Hanh H / Nguyen, Kambria / Nguyen, Thien H / Nieh, Angela W / Niu, Isabella / Oh, Seo-Kyung / Ong, Jessica R / Oyama, Randi K / Park, Joseph / Park, Yaelim A / Passmore, Kimberly A / Patel, Ami / Patel, Amy A / Patel, Dhruv / Patel, Tirth / Peterson, Katherine E / Pham, An Huynh / Pham, Steven V / Phuphanich, Melissa E / Poria, Neil D / Pourzia, Alexandra / Ragland, Victoria / Ranat, Riki D / Rice, Cameron M / Roh, David / Rojhani, Solomon / Sadri, Lili / Saguros, Agafe / Saifee, Zainab / Sandhu, Manjot / Scruggs, Brooke / Scully, Lisa M / Shih, Vanessa / Shin, Brian A / Sholklapper, Tamir / Singh, Harnek / Singh, Sumedha / Snyder, Sondra L / Sobotka, Katelyn F / Song, Sae Ho / Sukumar, Siddharth / Sullivan, Halley C / Sy, Mark / Tan, Hande / Taylor, Sara K / Thaker, Shivani K / Thakore, Tulsi / Tong, Gregory E / Tran, Jacinda N / Tran, Jonathan / Tran, Tuan D / Tran, Vivi / Trang, Cindy L / Trinh, Hung G / Trinh, Peter / Tseng, Han-Ching H / Uotani, Ted T / Uraizee, Akram V / Vu, Kent K T / Vu, Kevin K T / Wadhwani, Komal / Walia, Paluk K / Wang, Rebecca S / Wang, Shuo / Wang, Stephanie J / Wiredja, Danica D / Wong, Andrew L / Wu, Daniel / Xue, Xi / Yanez, Griselda / Yang, Yung-Hsuan / Ye, Zhong / Yee, Victor W / Yeh, Cynthia / Zhao, Yue / Zheng, Xin / Ziegenbalg, Anke / Alkali, Jon / Azizkhanian, Ida / Bhakta, Akash / Berry, Luke / Castillo, Ryen / Darwish, Sonja / Dickinson, Holly / Dutta, Ritika / Ghosh, Rahul Kumar / Guerin, Riley / Hofman, Jonathan / Iwamoto, Garrick / Kang, Sarah / Kim, Andrew / Kim, Brian / Kim, Hanwool / Kim, Kristine / Kim, Suji / Ko, Julie / Koenig, Michael / LaRiviere, Alejandro / Lee, Clifton / Lee, Jiwon / Lung, Brandon / Mittelman, Max / Murata, Mark / Park, Yujin / Rothberg, Daniel / Sprung-Keyser, Ben / Thaker, Kunal / Yip, Vivian / Picard, Paul / Diep, Francie / Villarasa, Nikki / Hartenstein, Volker / Shapiro, Casey / Levis-Fitzgerald, Marc / Jaworski, Leslie / Loppato, David / Clark, Ira E / Banerjee, Utpal

G3 (Bethesda, Md.)

2019 Volume 9, Issue 11, Page(s) 3791–3800

Abstract: A variety of genetic techniques have been devised to determine cell lineage relationships during tissue development. Some of these systems monitor cell lineages spatially and/or temporally without regard to gene expression by the cells, whereas others ... ...

Abstract	A variety of genetic techniques have been devised to determine cell lineage relationships during tissue development. Some of these systems monitor cell lineages spatially and/or temporally without regard to gene expression by the cells, whereas others correlate gene expression with the lineage under study. The
MeSH term(s)	Animals ; Brain ; Cell Lineage ; Drosophila/genetics ; Eye ; Gene Expression ; Lymphatic System ; Research ; Students ; Universities ; Wings, Animal
Language	English
Publishing date	2019-11-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2629978-1
ISSN	2160-1836 ; 2160-1836
ISSN (online)	2160-1836
ISSN	2160-1836
DOI	10.1534/g3.119.400541
Database	MEDical Literature Analysis and Retrieval System OnLINE

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