MUC2 Antibody (996/1) - BSA Free

Flow Cytometry: MUC2 Antibody (996/1) - BSA Free [NB120-11197]

Flow Cytometry: MUC2 Antibody (996/1) [NB120-11197] - Analysis of Allophycocyanin conjugate of NB120-11197. An intracellular stain was performed on HeLa cells with MUC2 (996/1) antibody NB120-11197APC (blue) and a matched isotype control NBP2-27287APC (orange). Cells were fixed with 4% PFA and then permeabli

Flow Cytometry: MUC2 Antibody (996/1) - BSA Free [NB120-11197]

Flow Cytometry: MUC2 Antibody (996/1) [NB120-11197] - Analysis of Allophycocyanin conjugate of NB120-11197. An intracellular stain was performed on NTERA-2 cells with MUC2 (996/1) antibody NB120-11197APC (blue) and a matched isotype control NBP2-27287APC (orange). Cells were fixed with 4% PFA and then permea

Flow (Intracellular): MUC2 Antibody (996/1) - BSA Free [NB120-11197]

Flow (Intracellular): MUC2 Antibody (996/1) [NB120-11197] - An intracellular stain was performed on HeLa cells with MUC2 Antibody (996/1) NB120-11197AF488 (blue) and a matched isotype control (orange). Cells were fixed with 4% PFA and then permeabilized with 0.1% saponin. Cells were incubated in an antibody dilution of 10 ug/mL for 30 minutes at room temperature. Both antibodies were conjugated to Alexa Fluor 488.

Immunohistochemistry-Paraffin: Mouse Monoclonal MUC2 Antibody (996/1) [NB120-11197] -

Immunohistochemistry-Paraffin: Mouse Monoclonal MUC2 Antibody (996/1) [NB120-11197] - Staining of mouse colon tissue using MUC2 Antibody. Colon, MUC2 -Green, DAPI-Blue. Antibody dilution - 1:100. Image from a verified customer review.

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] -

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] - MS-induced intestinal epithelium injury was CRHR1 dependent.Photomicrographs of hematoxylin & eosin (H&E) stained (A–E) & immunofluorescence of Mucin 2 (Muc2; mucous-forming protein) (F–J) in proximal colon in all experimental groups. Histological scores (K) were highest in MS, demonstrated injury in MS compared to control. Treatment with Antalarmin & Astressin prevented this MS-induced colonic injury, but not by Astressin-2 beta. Crypt length in μm (L) (red lines in photomicrographs A–E) & the number of Muc2+ goblet cells per crypt (M) were reduced by MS compared to control, & restored to control levels following Antalarmin & Astressin treatment. Astressin-2 beta did not prevent these MS-induced effects. Myeloperoxidase (MPO; μmol/mg protein) expression was increased in MS group & was reduced to a level similar to control by treatment with Antalarmin but not by treatment with Astressin or Astressin-2 beta (N). Western blot analysis of NF-kappa B showed an increase in the phosphorylated expression of NF-kappa B in MS, which was prevented by Antalarmin administration, but not by Astressin or Astressin-2 beta (O,P). Trans-cellular flux of HRP (ng/ml.cm2.min; Q) measured by Ussing Chamber was increased in MS & MS + Astressin-2 beta groups, compared to control, but not in MS + Antalarmin & MS + Astressin groups (P). Results are means, ±SD. p < 0.05 was considered significant. Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/srep46616), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] -

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] - MS-induced intestinal epithelium injury was CRHR1 dependent.Photomicrographs of hematoxylin & eosin (H&E) stained (A–E) & immunofluorescence of Mucin 2 (Muc2; mucous-forming protein) (F–J) in proximal colon in all experimental groups. Histological scores (K) were highest in MS, demonstrated injury in MS compared to control. Treatment with Antalarmin & Astressin prevented this MS-induced colonic injury, but not by Astressin-2 beta. Crypt length in μm (L) (red lines in photomicrographs A–E) & the number of Muc2+ goblet cells per crypt (M) were reduced by MS compared to control, & restored to control levels following Antalarmin & Astressin treatment. Astressin-2 beta did not prevent these MS-induced effects. Myeloperoxidase (MPO; μmol/mg protein) expression was increased in MS group & was reduced to a level similar to control by treatment with Antalarmin but not by treatment with Astressin or Astressin-2 beta (N). Western blot analysis of NF-kappa B showed an increase in the phosphorylated expression of NF-kappa B in MS, which was prevented by Antalarmin administration, but not by Astressin or Astressin-2 beta (O,P). Trans-cellular flux of HRP (ng/ml.cm2.min; Q) measured by Ussing Chamber was increased in MS & MS + Astressin-2 beta groups, compared to control, but not in MS + Antalarmin & MS + Astressin groups (P). Results are means, ±SD. p < 0.05 was considered significant. Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/srep46616), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] -

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] - MS-induced intestinal epithelium injury was CRHR1 dependent.Photomicrographs of hematoxylin & eosin (H&E) stained (A–E) & immunofluorescence of Mucin 2 (Muc2; mucous-forming protein) (F–J) in proximal colon in all experimental groups. Histological scores (K) were highest in MS, demonstrated injury in MS compared to control. Treatment with Antalarmin & Astressin prevented this MS-induced colonic injury, but not by Astressin-2 beta. Crypt length in μm (L) (red lines in photomicrographs A–E) & the number of Muc2+ goblet cells per crypt (M) were reduced by MS compared to control, & restored to control levels following Antalarmin & Astressin treatment. Astressin-2 beta did not prevent these MS-induced effects. Myeloperoxidase (MPO; μmol/mg protein) expression was increased in MS group & was reduced to a level similar to control by treatment with Antalarmin but not by treatment with Astressin or Astressin-2 beta (N). Western blot analysis of NF-kappa B showed an increase in the phosphorylated expression of NF-kappa B in MS, which was prevented by Antalarmin administration, but not by Astressin or Astressin-2 beta (O,P). Trans-cellular flux of HRP (ng/ml.cm2.min; Q) measured by Ussing Chamber was increased in MS & MS + Astressin-2 beta groups, compared to control, but not in MS + Antalarmin & MS + Astressin groups (P). Results are means, ±SD. p < 0.05 was considered significant. Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/srep46616), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] -

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] - MS-induced intestinal epithelium injury was CRHR1 dependent.Photomicrographs of hematoxylin & eosin (H&E) stained (A–E) & immunofluorescence of Mucin 2 (Muc2; mucous-forming protein) (F–J) in proximal colon in all experimental groups. Histological scores (K) were highest in MS, demonstrated injury in MS compared to control. Treatment with Antalarmin & Astressin prevented this MS-induced colonic injury, but not by Astressin-2 beta. Crypt length in μm (L) (red lines in photomicrographs A–E) & the number of Muc2+ goblet cells per crypt (M) were reduced by MS compared to control, & restored to control levels following Antalarmin & Astressin treatment. Astressin-2 beta did not prevent these MS-induced effects. Myeloperoxidase (MPO; μmol/mg protein) expression was increased in MS group & was reduced to a level similar to control by treatment with Antalarmin but not by treatment with Astressin or Astressin-2 beta (N). Western blot analysis of NF-kappa B showed an increase in the phosphorylated expression of NF-kappa B in MS, which was prevented by Antalarmin administration, but not by Astressin or Astressin-2 beta (O,P). Trans-cellular flux of HRP (ng/ml.cm2.min; Q) measured by Ussing Chamber was increased in MS & MS + Astressin-2 beta groups, compared to control, but not in MS + Antalarmin & MS + Astressin groups (P). Results are means, ±SD. p < 0.05 was considered significant. Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/srep46616), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] -

Immunocytochemistry/ Immunofluorescence: MUC2 Antibody (996/1) - BSA Free [NB120-11197] - MS-induced intestinal epithelium injury was CRHR1 dependent.Photomicrographs of hematoxylin & eosin (H&E) stained (A–E) & immunofluorescence of Mucin 2 (Muc2; mucous-forming protein) (F–J) in proximal colon in all experimental groups. Histological scores (K) were highest in MS, demonstrated injury in MS compared to control. Treatment with Antalarmin & Astressin prevented this MS-induced colonic injury, but not by Astressin-2 beta. Crypt length in μm (L) (red lines in photomicrographs A–E) & the number of Muc2+ goblet cells per crypt (M) were reduced by MS compared to control, & restored to control levels following Antalarmin & Astressin treatment. Astressin-2 beta did not prevent these MS-induced effects. Myeloperoxidase (MPO; μmol/mg protein) expression was increased in MS group & was reduced to a level similar to control by treatment with Antalarmin but not by treatment with Astressin or Astressin-2 beta (N). Western blot analysis of NF-kappa B showed an increase in the phosphorylated expression of NF-kappa B in MS, which was prevented by Antalarmin administration, but not by Astressin or Astressin-2 beta (O,P). Trans-cellular flux of HRP (ng/ml.cm2.min; Q) measured by Ussing Chamber was increased in MS & MS + Astressin-2 beta groups, compared to control, but not in MS + Antalarmin & MS + Astressin groups (P). Results are means, ±SD. p < 0.05 was considered significant. Image collected & cropped by CiteAb from the following publication (https://www.nature.com/articles/srep46616), licensed under a CC-BY license. Not internally tested by Novus Biologicals.