atcc htb 17 Search Results


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ATCC atcc htb 17
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ATCC kgp152 17 mda mb 231 luc cells
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ATCC progesterone receptorpositive breast cancer mcf7
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me180  (ATCC)
95
ATCC me180
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ATCC us cr ip t ac ce pt ed 17 human nci h460 nsclc
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ATCC u373 mg
Figure 2. ACSVL3 expression in cultured human glioma cells and xenografts correlates with RTK activation. A, human U87, <t>U373,</t> and Mayo 22 glioma cells were grown to ∼80% confluence. Cells were serum starved overnight and were incubated for 16 h in the absence or presence of HGF (20 ng/mL; a gift from Genentech) or EGF (30 ng/mL; Calbiochem/EMD) before harvesting and Western blot analysis for ACSVL3 expression. Each lane contained 30 μg of total cellular protein. B, U87 cells stably expressing constitutively active EGFR (EGFRvIII) or corresponding control U87 cells were harvested and analyzed by Western blot. C, tumors were produced in the flanks of athymic nude mice (n = 12) by s.c. injection (two sites per mouse) of 4 × 106 U87 cells. When tumor size reached ∼300 mm3 (day 14), animals were randomly divided into two groups of six mice. One group received i.p. injection (100 μg/20 g body weight) of anti-HGF mAb (L2G7) and the other group received isotype control mAb (5G8) on days 14, 16, and 18 (17). Mice were sacrificed on day 20. Tumor homogenates (50 μg of protein) were subjected to Western blot analysis for ACSVL3 expression. Actin expression was used as a loading control for all blots.
U373 Mg, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC protein 1 u373 mg atcc
Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, <t>U373</t> and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.
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ATCC caco 2 cell line
Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, <t>U373</t> and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.
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ATCC bt 474 cells
Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, <t>U373</t> and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.
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ATCC mda mb 134 vi
Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, <t>U373</t> and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.
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ATCC sk ov 3
Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, <t>U373</t> and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.
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ATCC a498 5 74 5 17 4 00 achn 5 49 4 00 4 00 caki
Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, <t>U373</t> and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.
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Image Search Results


Figure 2. ACSVL3 expression in cultured human glioma cells and xenografts correlates with RTK activation. A, human U87, U373, and Mayo 22 glioma cells were grown to ∼80% confluence. Cells were serum starved overnight and were incubated for 16 h in the absence or presence of HGF (20 ng/mL; a gift from Genentech) or EGF (30 ng/mL; Calbiochem/EMD) before harvesting and Western blot analysis for ACSVL3 expression. Each lane contained 30 μg of total cellular protein. B, U87 cells stably expressing constitutively active EGFR (EGFRvIII) or corresponding control U87 cells were harvested and analyzed by Western blot. C, tumors were produced in the flanks of athymic nude mice (n = 12) by s.c. injection (two sites per mouse) of 4 × 106 U87 cells. When tumor size reached ∼300 mm3 (day 14), animals were randomly divided into two groups of six mice. One group received i.p. injection (100 μg/20 g body weight) of anti-HGF mAb (L2G7) and the other group received isotype control mAb (5G8) on days 14, 16, and 18 (17). Mice were sacrificed on day 20. Tumor homogenates (50 μg of protein) were subjected to Western blot analysis for ACSVL3 expression. Actin expression was used as a loading control for all blots.

Journal: Cancer Research

Article Title: Acyl-CoA Synthetase VL3 Knockdown Inhibits Human Glioma Cell Proliferation and Tumorigenicity

doi: 10.1158/0008-5472.can-08-4689

Figure Lengend Snippet: Figure 2. ACSVL3 expression in cultured human glioma cells and xenografts correlates with RTK activation. A, human U87, U373, and Mayo 22 glioma cells were grown to ∼80% confluence. Cells were serum starved overnight and were incubated for 16 h in the absence or presence of HGF (20 ng/mL; a gift from Genentech) or EGF (30 ng/mL; Calbiochem/EMD) before harvesting and Western blot analysis for ACSVL3 expression. Each lane contained 30 μg of total cellular protein. B, U87 cells stably expressing constitutively active EGFR (EGFRvIII) or corresponding control U87 cells were harvested and analyzed by Western blot. C, tumors were produced in the flanks of athymic nude mice (n = 12) by s.c. injection (two sites per mouse) of 4 × 106 U87 cells. When tumor size reached ∼300 mm3 (day 14), animals were randomly divided into two groups of six mice. One group received i.p. injection (100 μg/20 g body weight) of anti-HGF mAb (L2G7) and the other group received isotype control mAb (5G8) on days 14, 16, and 18 (17). Mice were sacrificed on day 20. Tumor homogenates (50 μg of protein) were subjected to Western blot analysis for ACSVL3 expression. Actin expression was used as a loading control for all blots.

Article Snippet: Human U87 MG (ATCC #HTB-14) and U373 MG (ATCC #HTB-17) glioblastoma cell lines have been maintained in our laboratory for >10 y and were cultured as previously described (10).

Techniques: Expressing, Cell Culture, Activation Assay, Incubation, Western Blot, Stable Transfection, Control, Produced, Injection

Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, U373 and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.

Journal: Oncology letters

Article Title: miR-7-5p inhibits cell migration and invasion in glioblastoma through targeting SATB1.

doi: 10.3892/ol.2018.9777

Figure Lengend Snippet: Figure 1. Downregulation of miR‑7‑5p in human glioblastoma tissues and cell lines. (A) Expression of miR‑7‑5p in tumor tissues and non‑tumor tissues. (B) miR‑7‑5p expression in U87, U373 and NHAs (control). **P<0.01. NHAs, normal human astrocytes; miR, microRNA.

Article Snippet: China E‐mail: fvz755359@163.com *Contributed equally Key words: glioblastoma, microRNA‐7‐5p, migration, invasion, special AT rich sequence binding protein 1 U373 MG ATCC (male malignant gliomas, ATCC HTB‐17) as mixed astrocytoma cells were purchased from the ATCC and cultured in DMEM supplemented with 10% fetal bovine serum (FBS).

Techniques: Expressing, Control