42379 Search Results


gp96/hsp90b1/grp94 antibody (cl2647)  (Bio-Techne corporation)
91
Bio-Techne corporation gp96/hsp90b1/grp94 antibody (cl2647)
Gp96/Hsp90b1/Grp94 Antibody (Cl2647), supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/gp96/hsp90b1/grp94 antibody (cl2647)/product/Bio-Techne corporation
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
gp96/hsp90b1/grp94 antibody (cl2647) - by Bioz Stars, 2024-12
91/100 stars
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hsp90b1  (Novus Biologicals)
91
Novus Biologicals hsp90b1
(A) IP followed by WB analysis of JAK1, STT3A, and ngPD-L1 tyrosine phosphorylation (4G10) in FLAG–ngPD-L1–SK-HEP-1 cells with or without exposure to IL-6 (20 ng/mL) and ruxolitinib (10 μmol/L) for 30 minutes. (B) JAK1 interacts with ngPD-L1 in ER lumen. Representative images of individual immunofluorescence staining of JAK1 and PD-L1 interaction in ER region in Hep 3B cells by Duolink assay. The red dots (JAK1/PD-L1 interaction) indicate their interaction. Green fluorescence <t>(HSP90B1)</t> was used as ER marker, and DAPI as a nuclear marker. (C) Schematic showing JAK1/PD-L1 interaction in the ER. IC, intracellular domain; TM, transmembrane domain; EC, extracellular domain. (D) Trypsin digestion of ER fractions with (group 3) or without (group 2) permeabilization in Hep 3B cells.
Hsp90b1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hsp90b1/product/Novus Biologicals
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
hsp90b1 - by Bioz Stars, 2024-12
91/100 stars
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control shrna  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology control shrna
Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
Control Shrna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/control shrna/product/Santa Cruz Biotechnology
Average 90 stars, based on 1 article reviews
Price from $9.99 to $1999.99
control shrna - by Bioz Stars, 2024-12
90/100 stars
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short hairpin rna shrna  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology short hairpin rna shrna
Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
Short Hairpin Rna Shrna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/short hairpin rna shrna/product/Santa Cruz Biotechnology
Average 90 stars, based on 1 article reviews
Price from $9.99 to $1999.99
short hairpin rna shrna - by Bioz Stars, 2024-12
90/100 stars
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echinocandin  (ATCC)
90
ATCC echinocandin
Absence of chloride channel <t>protein-2</t> <t>(ClC-2)</t> resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA <t>(shRNA)</t> cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.
Echinocandin, supplied by ATCC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/echinocandin/product/ATCC
Average 90 stars, based on 1 article reviews
Price from $9.99 to $1999.99
echinocandin - by Bioz Stars, 2024-12
90/100 stars
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Image Search Results


(A) IP followed by WB analysis of JAK1, STT3A, and ngPD-L1 tyrosine phosphorylation (4G10) in FLAG–ngPD-L1–SK-HEP-1 cells with or without exposure to IL-6 (20 ng/mL) and ruxolitinib (10 μmol/L) for 30 minutes. (B) JAK1 interacts with ngPD-L1 in ER lumen. Representative images of individual immunofluorescence staining of JAK1 and PD-L1 interaction in ER region in Hep 3B cells by Duolink assay. The red dots (JAK1/PD-L1 interaction) indicate their interaction. Green fluorescence (HSP90B1) was used as ER marker, and DAPI as a nuclear marker. (C) Schematic showing JAK1/PD-L1 interaction in the ER. IC, intracellular domain; TM, transmembrane domain; EC, extracellular domain. (D) Trypsin digestion of ER fractions with (group 3) or without (group 2) permeabilization in Hep 3B cells.

Journal: The Journal of Clinical Investigation

Article Title: IL-6/JAK1 pathway drives PD-L1 Y112 phosphorylation to promote cancer immune evasion

doi: 10.1172/JCI126022

Figure Lengend Snippet: (A) IP followed by WB analysis of JAK1, STT3A, and ngPD-L1 tyrosine phosphorylation (4G10) in FLAG–ngPD-L1–SK-HEP-1 cells with or without exposure to IL-6 (20 ng/mL) and ruxolitinib (10 μmol/L) for 30 minutes. (B) JAK1 interacts with ngPD-L1 in ER lumen. Representative images of individual immunofluorescence staining of JAK1 and PD-L1 interaction in ER region in Hep 3B cells by Duolink assay. The red dots (JAK1/PD-L1 interaction) indicate their interaction. Green fluorescence (HSP90B1) was used as ER marker, and DAPI as a nuclear marker. (C) Schematic showing JAK1/PD-L1 interaction in the ER. IC, intracellular domain; TM, transmembrane domain; EC, extracellular domain. (D) Trypsin digestion of ER fractions with (group 3) or without (group 2) permeabilization in Hep 3B cells.

Article Snippet: After trypsinization, samples were analyzed by Western blotting using primary antibodies against IRE1α (3294; 1:2000; Cell Signaling Technology), HSP90B1 (catalog NBP2-42379; 1:3000; Novus Biologicals), or JAK1 (catalog 610231; 1:2000; BD Biosciences).

Techniques: Immunofluorescence, Staining, Fluorescence, Marker

Absence of chloride channel protein-2 (ClC-2) resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA (shRNA) cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.

Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

Article Title: Knockout of ClC-2 reveals critical functions of adherens junctions in colonic homeostasis and tumorigenicity

doi: 10.1152/ajpgi.00087.2018

Figure Lengend Snippet: Absence of chloride channel protein-2 (ClC-2) resulted in increased in vitro tumorigenicity and disrupted adherens junctions (AJ) proteins in HT-29 colon cancer cells. A: equal numbers of control (CT) and ClC-2 short-hairpin RNA (shRNA) cells were plated on a 96-well plate. Cell proliferation was monitored with the cell counting kit-8 (CCK-8) assay at different time points. Downregulated ClC-2 significantly increased HT-29 cell proliferation. B: in vitro tumorigenicity of the CT and ClC-2 shRNA cells was determined by a colony formation assay assessing anchorage-dependent and -independent cell populations. The tumorigenicity of ClC-2 shRNA cells was significantly increased compared with CT cells. C: ClC-2 knockdown induced disruption of AJ proteins E-cadherin and β-catenin. Arrowhead, nuclear distribution of β-catenin. D: proximity ligation assay (PLA) showing the interaction (red dots) between E-cadherin and β-catenin in ClC-2 shRNA cells was significantly reduced compared with ClC-2 wild type (WT). Data are presented as means ± SE. *P < 0.05, **P < 0.01, and ***P < 0.01 vs. CT shRNA, Student’s t-test.

Article Snippet: Persistent knockdown of clcn-2 gene expression using short-hairpin RNA (shRNA) was achieved by transfecting HT-29 cells with lentiviral particles encoding ClC-2 shRNA or control shRNA (catalog nos. sc-42379-V and sc-108080; Santa Cruz Biotechnology).

Techniques: In Vitro, shRNA, Cell Counting, CCK-8 Assay, Colony Assay, Proximity Ligation Assay