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Pan ras

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Pan RAS is a laboratory reagent that detects the presence of RAS proteins, which are a family of small GTPase proteins involved in cell signaling pathways. The product provides a tool for researchers to identify and study RAS proteins in biological samples.

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Lab products found in correlation

Total erk1 2, by Cell Signaling Technology (2 mentions) Total mek1 2, by Cell Signaling Technology (2 mentions) Pan trk clone a7h6r, by Cell Signaling Technology (2 mentions) Phospho trka y674 675 clone c50f3, by Cell Signaling Technology (2 mentions) Phospho plc y783, by Cell Signaling Technology (2 mentions) Phospho mek1 2 s217 221 clone 41g9, by Cell Signaling Technology (2 mentions) Braf clone d9t6s, by Cell Signaling Technology (2 mentions) Brafv600e, by Abcam (2 mentions) Phospho p44 42 mapk erk1 2 t202 y204 clone d13.14.4e, by Cell Signaling Technology (2 mentions) Phospho akt s473 clone d9e, by Cell Signaling Technology (2 mentions) β actin clone 13e5, by Cell Signaling Technology (2 mentions) Erk1 2, by Cell Signaling Technology (2 mentions) Phospho atm ser1981, by Rockland Immunochemicals (1 mentions) Phospho h2ax ser139, by Merck Group (1 mentions) Phospho chk2 thr68, by Cell Signaling Technology (1 mentions) Phospho chk1 ser345, by Cell Signaling Technology (1 mentions) Goat anti rabbit igg h l hrp, by Thermo Fisher Scientific (1 mentions) Hrp rabbit anti mouse igg h l, by Thermo Fisher Scientific (1 mentions) Rab27a, by Abcam (1 mentions) P erk1 2, by Cell Signaling Technology (1 mentions)

5 protocols using pan ras

1

Comprehensive Western Blot Analysis

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Western blots: total protein lysates following the indicated treatment were extracted and separated using SDS-PAGE gels according to standard methods. Membranes were probed using the following antibodies: pan Trk clone A7H6R (92991S Cell Signaling Technology), phospho TrkA (Y674/675) clone C50F3 (4621S Cell Signaling Technology), phospho PLCƔ (Y783; 2821L Cell Signaling Technology), phospho MEK1/2 (S217/221) clone 41G9 (9154S Cell Signaling Technology), total MEK1/2 (9122L Cell Signaling Technology), BRAF clone D9T6S (14814S Cell Signaling Technology), BRAF V600E (ab228461 Abcam), phospho p44/42 MAPK (Erk1/2; T202/Y204) clone D13.14.4E (4370S Cell Signaling Technology), total ERK1/2 (9102S Cell Signaling Technology), phospho AKT (S473) clone D9E (4060L Cell Signaling Technology), total AKT (9272S Cell Signaling Technology), pan RAS (BK008, part AESA02 Cytoskeleton), KRAS (F234 Santa Cruz) and β-actin clone 13E5 (4970S Cell Signaling Technology).
Cocco E., Schram A.M., Kulick A., Misale S., Won H.H., Yaeger R., Razavi P., Ptashkin R., Hechtman J.F., Toska E., Cownie J., Somwar R., Shifman S., Mattar M., Selçuklu S.D., Samoila A., Guzman S., Tuch B.B., Ebata K., de Stanchina E., Nagy R.J., Lanman R.B., Houck-Loomis B., Patel J.A., Berger M.F., Ladanyi M., Hyman D.M., Drilon A, & Scaltriti M. (2019). Resistance to TRK inhibition mediated by convergent MAP kinase pathway activation. Nature medicine, 25(9), 1422-1427.
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2

Comprehensive Western Blot Analysis

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Western blots: total protein lysates following the indicated treatment were extracted and separated using SDS-PAGE gels according to standard methods. Membranes were probed using the following antibodies: pan Trk clone A7H6R (92991S Cell Signaling Technology), phospho TrkA (Y674/675) clone C50F3 (4621S Cell Signaling Technology), phospho PLCƔ (Y783; 2821L Cell Signaling Technology), phospho MEK1/2 (S217/221) clone 41G9 (9154S Cell Signaling Technology), total MEK1/2 (9122L Cell Signaling Technology), BRAF clone D9T6S (14814S Cell Signaling Technology), BRAF V600E (ab228461 Abcam), phospho p44/42 MAPK (Erk1/2; T202/Y204) clone D13.14.4E (4370S Cell Signaling Technology), total ERK1/2 (9102S Cell Signaling Technology), phospho AKT (S473) clone D9E (4060L Cell Signaling Technology), total AKT (9272S Cell Signaling Technology), pan RAS (BK008, part AESA02 Cytoskeleton), KRAS (F234 Santa Cruz) and β-actin clone 13E5 (4970S Cell Signaling Technology).
Cocco E., Schram A.M., Kulick A., Misale S., Won H.H., Yaeger R., Razavi P., Ptashkin R., Hechtman J.F., Toska E., Cownie J., Somwar R., Shifman S., Mattar M., Selçuklu S.D., Samoila A., Guzman S., Tuch B.B., Ebata K., de Stanchina E., Nagy R.J., Lanman R.B., Houck-Loomis B., Patel J.A., Berger M.F., Ladanyi M., Hyman D.M., Drilon A, & Scaltriti M. (2019). Resistance to TRK inhibition mediated by convergent MAP kinase pathway activation. Nature medicine, 25(9), 1422-1427.
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3

Immunoblot Analysis of DNA Damage Proteins

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Immunoblot analysis was carried out as described previously.46, 47 Antibodies specific for the following were used: MCM834; MCM934; Pan‐RAS (sc‐166691; Santa Cruz Biotechnology, Dallas, TX, USA); p53 (OP43; Calbiochem, Dallas, TX, USA); Chk1 (sc‐8408; Santa Cruz Biotechnology); phospho‐Chk1 Ser345 (#2348S; Cell Signaling Technology, Danvers, MA, USA); Chk2 (#05‐649; Upstate, Lake Placid, NY, USA); phospho‐Chk2 Thr68 (#2661; Cell Signaling Technology); phospho‐H2AX Ser139 (#07‐164; Millipore, Burlington, MA, USA); phospho‐ATM Ser1981 (#20772; Rockland, Limerick, PA, USA); and Rad51 (70‐012; Bio Academia, Osaka, Japan). The following secondary Abs were used: HRP‐rabbit anti‐mouse IgG (H + L) (61‐6520; Invitrogen, Carlsbad, CA, USA); HRP‐goat anti‐rabbit IgG (H + L) (65‐6120; Invitrogen); Alexa 594‐conjugated donkey anti‐rabbit IgG (H + L) (A21207; Invitrogen); and Alexa 488‐conjugated goat anti‐mouse IgG (H + L) (A11029; Molecular Probes, Eugene, OR, USA).
Morii I., Iwabuchi Y., Mori S., Suekuni M., Natsume T., Yoshida K., Sugimoto N., Kanemaki M.T, & Fujita M. (2019). Inhibiting the MCM8‐9 complex selectively sensitizes cancer cells to cisplatin and olaparib. Cancer Science, 110(3), 1044-1053.
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4

Western Blot Analysis of Extracellular Vesicle Proteins

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Proteins derived from cells and EVs were resolved using sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS–PAGE), transferred onto nitrocellulose membranes, bound with primary antibodies, and incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies. Protein bands were visualized using enhanced chemiluminescence detection reagents (34580, Thermo Scientific, Waltham, MA, USA). Primary antibodies against the following proteins were used: Alix (ab56932, Abcam, Cambridge, UK), CD63 (ab68418, Abcam), TSG101 (ab56932, Abcam), Synthenin-1 (ab133267, Abcam), β-actin (112620, Cell Signaling Technology, Danvers, MA, USA), PD-L1 (13684, Cell Signaling Technology), Rab27a (ab55667, Abcam), Rab11 (ab18211, Abcam), Rab7 (ab50533, Abcam), pan Ras (sc-166691, Santa Cruz, Santa Cruz, CA, USA), Rap1A (sc-398755, Santa Cruz), p-B-Raf (2696S, Cell Signaling Technology), B-Raf (9433S, Cell Signaling Technology), p-MEK (9154S, Cell Signaling Technology), MEK (9126S, Cell Signaling Technology), p-ERK1/2 (4370S, Cell Signaling Technology), ERK1/2 (4695S, Cell Signaling Technology), p-AKT (4060S, Cell Signaling Technology), and AKT (9272S, Cell Signaling Technology).
Choe E.J., Lee C.H., Bae J.H., Park J.M., Park S.S, & Baek M.C. (2022). Atorvastatin Enhances the Efficacy of Immune Checkpoint Therapy and Suppresses the Cellular and Extracellular Vesicle PD-L1. Pharmaceutics, 14(8), 1660.
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5

Western Blot Analysis of Signaling Proteins

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Equal amounts of protein were separated by SDS-PAGE and transferred nitrocellulose membranes (Hybond-ECLTM, Amersham Bioscience). Membranes were blocked with 5% fat-free milk powder in PBS containing 0.1% Tween 20 for 2 h and incubated with specific antibodies against ERK 1/2 (Cell signalling), pERK 1/2 Thr202/Tyr204 (Cell signaling), GAPDH (Santa Cruz), MEK 1/2 (Santa Cruz), pMEK 1/2 Ser217/221 (Cell signaling), panRas (Santa Cruz), Raf 1 (Santa Cruz) and pRaf-1 Ser 338/Tyr 341 (Santa Cruz) over night at 4°C. Proteins were visualized by secondary antibodies conjugated to horseradish peroxidase (HRP) and freshly prepared ECL solution, containing 2.5 mM luminol (Supplementary Tables S3 and S4). Chemiluminescence signal was detected with the ChemiDocTM Touch Imaging System (Bio-Rad, Munich, Germany).
Bartel K., Winzi M., Ulrich M., Koeberle A., Menche D., Werz O., Müller R., Guck J., Vollmar A.M, & von Schwarzenberg K. (2016). V-ATPase inhibition increases cancer cell stiffness and blocks membrane related Ras signaling - a new option for HCC therapy. Oncotarget, 8(6), 9476-9487.
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