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The UAS-dMyc is a genetic construct that allows for the overexpression of the dMyc gene in Drosophila melanogaster. The dMyc gene is a homolog of the human c-Myc proto-oncogene and plays a role in cell growth and proliferation. The UAS-dMyc construct can be used in conjunction with the GAL4 transcriptional activator system to induce targeted overexpression of dMyc in specific cell types or developmental stages.

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Lab products found in correlation

Uas bskdn, by Bloomington Drosophila Stock Center (1 mentions) Uas timp, by Bloomington Drosophila Stock Center (1 mentions) Uas diap1, by Bloomington Drosophila Stock Center (1 mentions) Ab1 gal4, by Bloomington Drosophila Stock Center (1 mentions) Uas p35, by Bloomington Drosophila Stock Center (1 mentions) Uas gfp, by Bloomington Drosophila Stock Center (1 mentions) Uas 2xegfp, by Bloomington Drosophila Stock Center (1 mentions) W1118, by Bloomington Drosophila Stock Center (1 mentions) Uas gfp rnai, by Bloomington Drosophila Stock Center (1 mentions) Dmef2 gal4, by Bloomington Drosophila Stock Center (1 mentions) Wtsx1, by Bloomington Drosophila Stock Center (1 mentions) Uas jnkdn, by Bloomington Drosophila Stock Center (1 mentions) Uas rasv12, by Bloomington Drosophila Stock Center (1 mentions) Uas yki v5, by Bloomington Drosophila Stock Center (1 mentions) 30a gal4, by Bloomington Drosophila Stock Center (1 mentions) Nub gal4, by Bloomington Drosophila Stock Center (1 mentions) Uas mir 277 sponge, by Bloomington Drosophila Stock Center (1 mentions)

4 protocols using uas dmyc

1

Overexpression of Salr, Salm, and SALL4 in Drosophila

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Fly lines were cultured at 25°C on standard fly food unless otherwise noted. The transgenes used were as follows: UAS-salr (de Celis et al., 1996 (link)), UAS-salm (from the Bloomington Drosophila Stock Center #29716, short for BL#29716), UAS-SALL4-HA (BL#65835), UAS-Timp (BL#58708), UAS-bskDN (Weber et al., 2000 (link)), UAS-p35 (BL#5073), UAS-Diap1 (BL#6657), UAS-GFP (nuclear expression, BL#4775), UAS-CD8-GFP (membrane expression) (Lee and Luo, 1999 (link)), UAS-dMyc (BL#9674), dMyc-RNAi (BL#36123), puc-lacZ (Martin-Blanco et al., 1998 (link)), UAS-puc (Dobens et al., 2001 (link)), dpp-Gal4 (Shen and Mardon, 1997 (link)), actin5c>CD2>Gal4 (Pignoni and Zipursky, 1997 (link)), and AB1-Gal4 (BL#1824). To promote the GFP phenotype in a larval body, salm, salr, or SALL4-overexpressing larvae were raised at 29°C after egg laying. Clones in the larval wing imaginal discs were generated with the genotypes y w1118 hs-Flp; actin5c>CD2>Gal4 UAS-GFP/CyO; UAS-salr/UAS-SALL4-HA by heat shock at 35.5°C for 30 min. Then, late third-instar larvae were dissected after a recovery period of 3 days at 25°C.
Sun J., Zhang J., Wang D, & Shen J. (2020). The transcription factor Spalt and human homologue SALL4 induce cell invasion via the dMyc-JNK pathway in Drosophila. Biology Open, 9(3), bio048850.
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2

Drosophila Larval Development Protocol

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The following Drosophila stocks were maintained under standard laboratory conditions (25 °C) on BDSC cornmeal medium (Bloomington Drosophila Stock Center: https://bdsc.indiana.edu/information/recipes/bloomfood.html): w1118 (Bloomington 3605), Dmef2-GAL4 (Ranganayakulu et al., 1998 (link)), UAS-2xEGFP (Bloomington 6874), UAS-GFP RNAi (from J. Zallen, SKI), UAS-dmyc (from N. Perrimon), UAS-dup (double parked/Ctd1) RNAi (from T. Orr-Weaver). Crosses (GAL4 × UAS) were performed at 25 °C on apple juice plates under 12:12 Light:Dark conditions and constant humidity. For all experiments, embryos hatched within a 2h period were selected and raised to third instar larval stage on cornmeal medium at 25°C. Staging of 3rd instar larvae was confirmed using developmental landmarks, including mouth hook and spiracle morphologies. Both male and female larvae were analyzed.
Windner S.E., Manhart A., Brown A., Mogilner A, & Baylies M.K. (2019). Nuclear scaling is coordinated among individual nuclei in multinucleated muscle fibers. Developmental cell, 49(1), 48-62.e3.
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3

Drosophila Genetic Toolkit for Research

Cited 1 time
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Stocks used in this study include the following: hsFLP; act<stop<Gal4, UAS-ykiS168A.v5, hsFLP;act<stop<Gal4, UAS-RFPNLS, hsFLP, UAS-GFPNLS; tub-Gal80, FRT40A (MARCM FRT 40A), ubi>RFP, FRT40A, banΔ1, banGFP, en-Gal4, dpp-lacZ, UAS-RFP, AP-1-RFP (53 (link)), and TIE-DYE (50 (link)). Stocks were obtained from the Bloomington Drosophila Stock Center (BDSC): UAS-ykiS168A.v5 (#28818), UAS-yki.v5 (#28819), UAS-yki::GFP (#28815), wtsX1 (#44251), smo3 (#3277), UAS-ciRNAi (#64928), tara1-lacZ (#6403), UAS-taraRNAi (#31634), nub-Gal4 (#42699), 30A-Gal4 (#37534), UAS-dMyc (#9674), UAS-rasv12 (#4847), and UAS-jnkDN (#9311). Ci-lacZ was a gift from D. Kalderon (Columbia University, USA). UAS-bantamsponge and UAS-bantam.D were gifts from S. Cohen (University of Copenhagen, Denmark). hs-Pc-sensor was a gift from V. Pirrotta (Rutgers University, USA). UAS-myc::tara was a gift from R. Smith-Bolton [University of Illinois, Urbana-Champaign, USA (originally from M. Cleary, University of California, Merced, USA)]. MARCM FRT19A and sd47M, FRT19A were gifts from D. Pan.
Bairzin J.C., Emmons-Bell M, & Hariharan I.K. (2020). The Hippo pathway coactivator Yorkie can reprogram cell fates and create compartment-boundary–like interactions at clone margins. Science Advances, 6(50), eabe8159.
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4

Drosophila Genetic Manipulation Protocol

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Flies were obtained from the Bloomington Drosophila Stock Center: UAS-dmyc (#7118); UAS-miR-277 (#36559); UAS-miR-277sponge (#61408). These Fly lines carrying UAS-RNA interference (RNAi) constructs were obtained from the Tsinghua Fly Center: dmycRNAi (#47953); imdRNAi (#31706); Tab2RNAi (#24667). As well as previously purchased tubulin-Gal80ts;TM2/TM6B (#7019) and tubulin-Gal4/TM3, Sb1, Ser1 (#5138), all flies were raised on maize malt molasses food in a light-dark (12-hr cycle) incubator at 25°C and 60% humidity. Flies were shifted to 30°C 24 h prior to and then during infection for UAS-protein/UAS-miR-277sponge/UAS-proteinRNAi overexpression experiments.
Li R., Zhou H., Jia C., Jin P, & Ma F. (2020). Drosophila Myc restores immune homeostasis of Imd pathway via activating miR-277 to inhibit imd/Tab2. PLoS Genetics, 16(8), e1008989.
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