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Nstr2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ntsr2  (Novus Biologicals)
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Relative transcript expression levels of genes expressing neurotensin ( NTS , A ), neurotensin receptor types 1 ( NTSR1 , B ) and 2 ( <t>NTSR2</t> , C ), and PCSK1 (panel D ) in FL-HCCs (T) versus paired, normal liver (N). ( E ) Immunoblotting demonstrates expression of NTS, NTSR1, NTSR2, and PCSK1 proteins in FL-HCCs (T) vs normal livers (N). HepG2 cells ( H ) were use as positive controls. ( F ) Low (10x) and high (100x) power magnification of FL-HCCs following immunohistochemical staining for NTS, NTSR1, NTSR2, or PCSK1.
Ntsr2, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/ntsr2/product/Novus Biologicals
Average 94 stars, based on 1 article reviews
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94/100 stars
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Relative transcript expression levels of genes expressing neurotensin ( NTS , A ), neurotensin receptor types 1 ( NTSR1 , B ) and 2 ( NTSR2 , C ), and PCSK1 (panel D ) in FL-HCCs (T) versus paired, normal liver (N). ( E ) Immunoblotting demonstrates expression of NTS, NTSR1, NTSR2, and PCSK1 proteins in FL-HCCs (T) vs normal livers (N). HepG2 cells ( H ) were use as positive controls. ( F ) Low (10x) and high (100x) power magnification of FL-HCCs following immunohistochemical staining for NTS, NTSR1, NTSR2, or PCSK1.

Journal: Oncotarget

Article Title: Neurotensin as a source of cyclic AMP and co-mitogen in fibrolamellar hepatocellular carcinoma

doi: 10.18632/oncotarget.27149

Figure Lengend Snippet: Relative transcript expression levels of genes expressing neurotensin ( NTS , A ), neurotensin receptor types 1 ( NTSR1 , B ) and 2 ( NTSR2 , C ), and PCSK1 (panel D ) in FL-HCCs (T) versus paired, normal liver (N). ( E ) Immunoblotting demonstrates expression of NTS, NTSR1, NTSR2, and PCSK1 proteins in FL-HCCs (T) vs normal livers (N). HepG2 cells ( H ) were use as positive controls. ( F ) Low (10x) and high (100x) power magnification of FL-HCCs following immunohistochemical staining for NTS, NTSR1, NTSR2, or PCSK1.

Article Snippet: Equal amounts of protein were separated by SDS-PAGE, transferred to Immobilon-P membranes (Millipore, Bedford, MA) and incubated at 4 degrees C overnight with the following primary antibodies: NTS (sc-20806, Santa Cruz), NTSR1 (sc-376958, Santa Cruz), NTSR2 (NB100-56472, Novus Biologicals), PCSK1 (sc-100578, Santa Cruz), phospho-p70 S6 Kinase (Thr389, #97596), phospho-p42/44 (#4370), phospho-MEK1/2 (Ser217/221, #9154), phospho-Src (Tyr416, #2101), phospho-EGFR (Tyr1068, #3777), phospho-HER2 (Tyr1248, #2247; all Cell Signaling) and β-Actin (A5441, Sigma, St. Louis, MO).

Techniques: Expressing, Western Blot, Immunohistochemical staining, Staining

JMV/EGF-stimulated AML12 cell proliferation was blocked by pretreatment with an inhibitor to NTSR1 (SF46892, A ), but not NTSR2 (NTFC824, B ). Either EGFR (AG213, C ) or MEK (cobemetinib, D ) inhibition block the proliferative effects of JMV/EGF treatment in AML12 cells. ( E ) Neither pre-treatment with NTSR1 (SR46892) or NTSR2 (NTFC824) inhibitors change ERK1/2 phosphorylation in response to EGF/JMV treatment. ( F ) Inhibition of EGF (erlotinib) or MEK (cobimetinib) decreases ERK1/2 phosphorylation in response to JMV and EGF; PI3K inhibition (wortmannin) does not affect ERK1/2 activation. Activation levels of Akt, EGFR, total S6, and MEK are also shown, with Actin serving as a loading control.

Journal: Oncotarget

Article Title: Neurotensin as a source of cyclic AMP and co-mitogen in fibrolamellar hepatocellular carcinoma

doi: 10.18632/oncotarget.27149

Figure Lengend Snippet: JMV/EGF-stimulated AML12 cell proliferation was blocked by pretreatment with an inhibitor to NTSR1 (SF46892, A ), but not NTSR2 (NTFC824, B ). Either EGFR (AG213, C ) or MEK (cobemetinib, D ) inhibition block the proliferative effects of JMV/EGF treatment in AML12 cells. ( E ) Neither pre-treatment with NTSR1 (SR46892) or NTSR2 (NTFC824) inhibitors change ERK1/2 phosphorylation in response to EGF/JMV treatment. ( F ) Inhibition of EGF (erlotinib) or MEK (cobimetinib) decreases ERK1/2 phosphorylation in response to JMV and EGF; PI3K inhibition (wortmannin) does not affect ERK1/2 activation. Activation levels of Akt, EGFR, total S6, and MEK are also shown, with Actin serving as a loading control.

Article Snippet: Equal amounts of protein were separated by SDS-PAGE, transferred to Immobilon-P membranes (Millipore, Bedford, MA) and incubated at 4 degrees C overnight with the following primary antibodies: NTS (sc-20806, Santa Cruz), NTSR1 (sc-376958, Santa Cruz), NTSR2 (NB100-56472, Novus Biologicals), PCSK1 (sc-100578, Santa Cruz), phospho-p70 S6 Kinase (Thr389, #97596), phospho-p42/44 (#4370), phospho-MEK1/2 (Ser217/221, #9154), phospho-Src (Tyr416, #2101), phospho-EGFR (Tyr1068, #3777), phospho-HER2 (Tyr1248, #2247; all Cell Signaling) and β-Actin (A5441, Sigma, St. Louis, MO).

Techniques: Inhibition, Blocking Assay, Phospho-proteomics, Activation Assay, Control