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rabbit anti-human jag1 (Cell Signaling Technology Inc)

Name: rabbit anti-human jag1
Brand: Cell Signaling Technology Inc
Rating: 90 (1 reviews)

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Cell Signaling Technology Inc rabbit anti-human jag1
Rabbit Anti Human Jag1, supplied by Cell Signaling Technology Inc, 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/rabbit anti-human jag1/product/Cell Signaling Technology Inc
Average 90 stars, based on 1 article reviews

rabbit anti-human jag1 - by Bioz Stars, 2026-02

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(A-D) Human Normal Astrocytes (NA) were seeded and cultured until confluence and starved for 24 h. NA were then treated for 24h with PBS 1X (control condition) versus 10 ng/mL of recombinant IL-1β (test condition). (A) DLL4 and (B) TYMP expression were then quantified by qRT-PCR. β -ACTIN was used as a reference. (C) Representative western blot for DLL4 and β-ACTIN protein expression level are shown. (D) DLL4 protein expression level was quantified by western blot. β-ACTIN was used as a reference. (E-H) 12-week-old C57Bl/6 females (4 animals per group) were induced with MOG 35-55 EAE versus Placebo. At day 13 post induction, mice were sacrificed and spinal cord neurovascular units were isolated. (E) Dll4 , (F) Hey1 , and (G) Jag1 expression were measured via qRT-PCR in both groups (MOG 35-55 versus placebo). (H) Spinal cord sections were harvested from MOG 35-55 EAE induced versus Placebo treated C57Bl/6 females and immune-stained with anti-DLL4 (in green) and anti-GFAP (in red) antibodies. Representative DLL4/GFAP staining is shown. (I) Human cortical sections from healthy donors and patients with cortical multiple sclerosis lesions were obtain from the NeuroCEB biobank and immunostained with anti-DLL4 (in green) and anti-GFAP (in red) antibodies. Nuclei were stained with DAPI (in blue). Representative DLL4/GFAP staining is shown. Mann-Whitney U test.

Journal: bioRxiv

Article Title: Juxtacrine DLL4-NOTCH1 signaling between astrocytes drives neuroinflammation via the IL-6-STAT3 axis

doi: 10.1101/2023.10.04.560826

Figure Lengend Snippet: (A-D) Human Normal Astrocytes (NA) were seeded and cultured until confluence and starved for 24 h. NA were then treated for 24h with PBS 1X (control condition) versus 10 ng/mL of recombinant IL-1β (test condition). (A) DLL4 and (B) TYMP expression were then quantified by qRT-PCR. β -ACTIN was used as a reference. (C) Representative western blot for DLL4 and β-ACTIN protein expression level are shown. (D) DLL4 protein expression level was quantified by western blot. β-ACTIN was used as a reference. (E-H) 12-week-old C57Bl/6 females (4 animals per group) were induced with MOG 35-55 EAE versus Placebo. At day 13 post induction, mice were sacrificed and spinal cord neurovascular units were isolated. (E) Dll4 , (F) Hey1 , and (G) Jag1 expression were measured via qRT-PCR in both groups (MOG 35-55 versus placebo). (H) Spinal cord sections were harvested from MOG 35-55 EAE induced versus Placebo treated C57Bl/6 females and immune-stained with anti-DLL4 (in green) and anti-GFAP (in red) antibodies. Representative DLL4/GFAP staining is shown. (I) Human cortical sections from healthy donors and patients with cortical multiple sclerosis lesions were obtain from the NeuroCEB biobank and immunostained with anti-DLL4 (in green) and anti-GFAP (in red) antibodies. Nuclei were stained with DAPI (in blue). Representative DLL4/GFAP staining is shown. Mann-Whitney U test.

Article Snippet: Anti β-ACTIN (rabbit), anti-CASP3 (rabbit) and Cleaved CASP3 (rabbit), anti-cleaved NOTCH1 (NICD) (rabbit), anti-DLL4 (rabbit), anti-human-JAG1 (rabbit), anti-P42-44 MAPK (rabbit) and phospho-P42-44 MAPK (rabbit), and anti-VIM (rabbit) were from cell signaling (Danvers, MA, USA).

Techniques: Cell Culture, Control, Recombinant, Expressing, Quantitative RT-PCR, Western Blot, Isolation, Staining, MANN-WHITNEY

(A-C) human Normal Astrocytes (NA) were seeded and cultured until 70% confluence. They were then transfected with a CONTROL siRNA (20µM) versus a DLL4 siRNA (20 µM), starved for 12 hours and treated with IL-1β 10ng/mL for 12h. The experiment was repeated 3×. (A-C) DLL4 expression was quantified by (A) qRT-PCR and (B-C) western blot. β-ACTIN was used as a reference. (B) Representative western blot for DLL4 and β-ACTIN protein expression level are shown. (C) DLL4 protein expression level was quantified. (D-H) Human Normal Astrocytes (NA) were seeded and cultured until 70% confluency. They were then treated as above and (D-E) JAG1, (D, F) NICD, (D, G) GFAP, and (D, H) cleaved CASP3 expression were quantified by western blot. β-ACTIN and CASP3 total were used as references. (I) Spinal cord sections were harvested from MOG 35-55 EAE induced Dll4ACKO1 mice and control littermates at 18 days post induction. Transcriptional RNA profiling of spinal cord lysates was performed and a Heatmap generated showing the list of genes involved in astrogliosis whose expression is different in both groups. (J-K) VIM and LCN2 protein expression were then quantified by western blot in spinal cord lysates from 10 weeks old C57BL/6 mice and EAE induced Dll4ACKO1 mice, Dll4ACKO2 mice and control littermates (at 18 days post induction). β-ACTIN was used as a reference. (J-K) Representative western blot for VIM, LCN2 and β-ACTIN in spinal cord lysates from (J) 10 weeks old C57BL/6 mice and EAE induced Dll4 ACKO P mice versus controls and (K) EAE induced Dll4 ACKO C mice versus controls are shown. (L-N) Spinal cord EAE lesions from Dll4 ACKO P mice, Dll4 ACKO C mice and littermate controls were harvested at 18 days post induction and tissues were immune-stained with anti-GFAP (in green), anti-VIM (in red) and anti PODXL (in grey) antibodies. Nuclei were stained with DAPI (in blue). (L) Dll4 ACKO C mice versus control tissues are shown. (M) GFAP+ and (N) VIM+/PODXL-areas were quantified ( Dll4 ACKO P mice n = 6, WT n = 6), (O) ( Dll4 ACKO C mice n = 7, WT n = 7)). Mann-Whitney U test or Kruskal Wallis test.

Journal: bioRxiv

Article Title: Juxtacrine DLL4-NOTCH1 signaling between astrocytes drives neuroinflammation via the IL-6-STAT3 axis

doi: 10.1101/2023.10.04.560826

Figure Lengend Snippet: (A-C) human Normal Astrocytes (NA) were seeded and cultured until 70% confluence. They were then transfected with a CONTROL siRNA (20µM) versus a DLL4 siRNA (20 µM), starved for 12 hours and treated with IL-1β 10ng/mL for 12h. The experiment was repeated 3×. (A-C) DLL4 expression was quantified by (A) qRT-PCR and (B-C) western blot. β-ACTIN was used as a reference. (B) Representative western blot for DLL4 and β-ACTIN protein expression level are shown. (C) DLL4 protein expression level was quantified. (D-H) Human Normal Astrocytes (NA) were seeded and cultured until 70% confluency. They were then treated as above and (D-E) JAG1, (D, F) NICD, (D, G) GFAP, and (D, H) cleaved CASP3 expression were quantified by western blot. β-ACTIN and CASP3 total were used as references. (I) Spinal cord sections were harvested from MOG 35-55 EAE induced Dll4ACKO1 mice and control littermates at 18 days post induction. Transcriptional RNA profiling of spinal cord lysates was performed and a Heatmap generated showing the list of genes involved in astrogliosis whose expression is different in both groups. (J-K) VIM and LCN2 protein expression were then quantified by western blot in spinal cord lysates from 10 weeks old C57BL/6 mice and EAE induced Dll4ACKO1 mice, Dll4ACKO2 mice and control littermates (at 18 days post induction). β-ACTIN was used as a reference. (J-K) Representative western blot for VIM, LCN2 and β-ACTIN in spinal cord lysates from (J) 10 weeks old C57BL/6 mice and EAE induced Dll4 ACKO P mice versus controls and (K) EAE induced Dll4 ACKO C mice versus controls are shown. (L-N) Spinal cord EAE lesions from Dll4 ACKO P mice, Dll4 ACKO C mice and littermate controls were harvested at 18 days post induction and tissues were immune-stained with anti-GFAP (in green), anti-VIM (in red) and anti PODXL (in grey) antibodies. Nuclei were stained with DAPI (in blue). (L) Dll4 ACKO C mice versus control tissues are shown. (M) GFAP+ and (N) VIM+/PODXL-areas were quantified ( Dll4 ACKO P mice n = 6, WT n = 6), (O) ( Dll4 ACKO C mice n = 7, WT n = 7)). Mann-Whitney U test or Kruskal Wallis test.

Techniques: Cell Culture, Transfection, Control, Expressing, Quantitative RT-PCR, Western Blot, Generated, Staining, MANN-WHITNEY

Journal: Molecular cell

Article Title: Systematic Characterization of Mutations Altering Protein Degradation in Human Cancers

doi: 10.1016/j.molcel.2021.01.020

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Rabbit monoclonal anti-human/mouse JAG1 , Cell Signaling Technology , Cat#70109.

Techniques: Control, Virus, Recombinant, In Vitro, Transfection, Western Blot, Capsules, Purification, Gel Extraction, cDNA Synthesis, RNA HS Assay, Plasmid Preparation, BIA-KA, Software, Adhesive

Journal: Aging (Albany NY)

Article Title: Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma

doi: 10.18632/aging.203979

Figure Lengend Snippet: Protein quantification results.

Article Snippet: The following primary antibodies were used: rabbit anti-human CCNB2 antibody (Abcam, USA) and rabbit anti-human JAG1 antibody (CST, USA).

Techniques:

Western blot was used to detect the interaction between CCNB2 protein and JAG1 protein in the tumor tissues of nude mice.

Journal: Aging (Albany NY)

Article Title: Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma

doi: 10.18632/aging.203979

Figure Lengend Snippet: Western blot was used to detect the interaction between CCNB2 protein and JAG1 protein in the tumor tissues of nude mice.

Article Snippet: The following primary antibodies were used: rabbit anti-human CCNB2 antibody (Abcam, USA) and rabbit anti-human JAG1 antibody (CST, USA).

Techniques: Western Blot

Overexpression of JAG1 restores the inhibition of proliferation and migration caused by knockdown of CCNB2. ( A ) The over-expression efficiency of JAG1 was detected by qPCR. ( B ) Western blot was used to observe the over-expression efficiency of JAG1 protein. ( C ) CCK-8 assays were performed after cell infection in Huh-7 cells. ( D ) Transwell assay observed the number of migratory cells in each group after Huh-7 cell infection. ( E ) Huh-7 migratory cells were detected by transwell assay. *p < 0.05, **p < 0.01.

Journal: Aging (Albany NY)

Article Title: Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma

doi: 10.18632/aging.203979

Figure Lengend Snippet: Overexpression of JAG1 restores the inhibition of proliferation and migration caused by knockdown of CCNB2. ( A ) The over-expression efficiency of JAG1 was detected by qPCR. ( B ) Western blot was used to observe the over-expression efficiency of JAG1 protein. ( C ) CCK-8 assays were performed after cell infection in Huh-7 cells. ( D ) Transwell assay observed the number of migratory cells in each group after Huh-7 cell infection. ( E ) Huh-7 migratory cells were detected by transwell assay. *p < 0.05, **p < 0.01.

Article Snippet: The following primary antibodies were used: rabbit anti-human CCNB2 antibody (Abcam, USA) and rabbit anti-human JAG1 antibody (CST, USA).

Techniques: Over Expression, Inhibition, Migration, Knockdown, Western Blot, CCK-8 Assay, Infection, Transwell Assay

JAG1 is overexpressed in HCC tissues. ( A ) Immunohistochemistry showed the expression of JAG1 in HCC and adjacent tissues. ( B ) The expression level of JAG1 was significantly higher in HCC tissues than in adjacent tissues. **p < 0.01.

Journal: Aging (Albany NY)

Article Title: Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma

doi: 10.18632/aging.203979

Figure Lengend Snippet: JAG1 is overexpressed in HCC tissues. ( A ) Immunohistochemistry showed the expression of JAG1 in HCC and adjacent tissues. ( B ) The expression level of JAG1 was significantly higher in HCC tissues than in adjacent tissues. **p < 0.01.

Article Snippet: The following primary antibodies were used: rabbit anti-human CCNB2 antibody (Abcam, USA) and rabbit anti-human JAG1 antibody (CST, USA).

Techniques: Immunohistochemistry, Expressing

Relationship between JAG1 and clinicopathological features of HCC patients(n=82).

Journal: Aging (Albany NY)

Article Title: Cyclin B2 overexpression promotes tumour growth by regulating jagged 1 in hepatocellular carcinoma

doi: 10.18632/aging.203979

Figure Lengend Snippet: Relationship between JAG1 and clinicopathological features of HCC patients(n=82).

Article Snippet: The following primary antibodies were used: rabbit anti-human CCNB2 antibody (Abcam, USA) and rabbit anti-human JAG1 antibody (CST, USA).

Techniques:

Expression profiles of genes involved in Notch signaling in X. laevis intestine during natural and T3‐induced metamorphosis. Quantitative real‐time RT‐PCR was performed using total RNAs prepared from the intestine of animals at indicated developmental stages ( A, C, E, G, I, K, M) or stage‐54 tadpoles after 10 nM T3 treatment ( B, D, F, H, J, L, N ). Levels of Hairy1 ( A, B ), Hairy2b ( C, D ), DLL1 ( E, F ), DLL3 ( G, H ), Jag1 ( I, J ), Jag2 ( K, L ), and Notch1 ( M, N ) mRNAs are shown relative to those of ribosomal protein L8 (rpL8) mRNA, with the values at stage 54 or 0‐day treatment set to 1. Error bars represent the SEM ( n = 7 for A–D ; n = 3 for E–H , J, M, N ; n = 8 for I, L ; n = 5 for K ). The values were analyzed by ANOVA followed by Scheffe's post hoc test whose results are shown only for the adjacent stages or days except for Notch1 ( M ). Asterisks indicate that the mRNA levels are significantly different. *, p < .05, **, p < .01; ns: not significant.

Journal: Stem Cells (Dayton, Ohio)

Article Title: Thyroid Hormone‐Induced Activation of Notch Signaling is Required for Adult Intestinal Stem Cell Development During Xenopus Laevis Metamorphosis

doi: 10.1002/stem.2544

Figure Lengend Snippet: Expression profiles of genes involved in Notch signaling in X. laevis intestine during natural and T3‐induced metamorphosis. Quantitative real‐time RT‐PCR was performed using total RNAs prepared from the intestine of animals at indicated developmental stages ( A, C, E, G, I, K, M) or stage‐54 tadpoles after 10 nM T3 treatment ( B, D, F, H, J, L, N ). Levels of Hairy1 ( A, B ), Hairy2b ( C, D ), DLL1 ( E, F ), DLL3 ( G, H ), Jag1 ( I, J ), Jag2 ( K, L ), and Notch1 ( M, N ) mRNAs are shown relative to those of ribosomal protein L8 (rpL8) mRNA, with the values at stage 54 or 0‐day treatment set to 1. Error bars represent the SEM ( n = 7 for A–D ; n = 3 for E–H , J, M, N ; n = 8 for I, L ; n = 5 for K ). The values were analyzed by ANOVA followed by Scheffe's post hoc test whose results are shown only for the adjacent stages or days except for Notch1 ( M ). Asterisks indicate that the mRNA levels are significantly different. *, p < .05, **, p < .01; ns: not significant.

Article Snippet: The sections of the intestine from stage‐62 tadpoles were double‐immunostained with a mixture of the mouse anti‐human cytokeratin 19 (CK19) (1:100; Novocastra), which is a predominant cytokeratin in the adult Ep including the stem cells , and the rabbit anti‐human DLL1 (1:100; Abcam, Tokyo, Japan), the rabbit anti‐human Jag1 (1:50; Santa Cruz Biotechnology, Dallas, TX), or the rabbit anti‐human Notch1 (1:500; Rockland Inc., Gilbertsville, PA).

Techniques: Expressing, Quantitative RT-PCR

Correlation of the expression patterns of Notch pathway components with that of a stem/progenitor marker in the metamorphosing intestine. Cross‐sections of the intestine from tadpoles at stages 60 ( A, D ) and 61 ( B, E, G, I ), and stage‐54 tadpoles treated with 10 nM T3 for 3 ( C, F ) and 5 days ( H, J ) were hybridized with antisense Hairy1 ( A‐C ) or Hairy2b ( G, H ) probes. The corresponding serial sections were hybridized with antisense LGR5 probe ( D–F, I, J ) for comparison. Hairy1 is expressed in the adult epithelial stem (AE)/progenitor cells (A, arrowhead) when they first appear as the small islets expressing LGR5 ( D , arrow) at stage 60. These islets grew in size as metamorphosis proceeded and continued to co‐express Hairy1 ( B , arrowheads) and LGR5 ( E , arrows). During T3‐induced metamorphosis, Hairy1 ( C , arrowhead) is also expressed in the AE/progenitor cells expressing LGR5 ( F , arrow) after 3 days of T3 treatment. Some, although not all, cells expressing Hairy2b were in the connective tissue (CT) ( G , arrowheads) underlying the AE/progenitor cells expressing LGR5 ( I , arrows). Hairy2b is also expressed in the CT after 5 days of T3 treatment ( H , arrowheads), again, with some underlying the AE/progenitor cells ( J , arrows). Cross‐sections of the intestine from tadpoles at stage 62 were double‐immunostained with anti‐CK19 to detect the islet of AE/progenitor cells ( K–M , red) and anti‐DLL1 ( K , green), anti‐Jag1 ( L , green), or anti‐Notch1 ( M , green) followed by counterstaining with DAPI ( K–M , blue). DLL1 ( K , arrowheads) and Notch1 ( M , arrowheads) are expressed in the islets (arrows). The cells expressing Jag1 are scattered in both the larval Ep and CT with some just beneath the islet, but not in the islets ( L , arrowheads). The dashed‐lines indicate the boundary of the Ep and the CT. Scale bars = 20 μm. Abbreviations: AE, adult epithelial stem/progenitor cells, CT, connective tissue, Ep, epithelium.

Journal: Stem Cells (Dayton, Ohio)

Article Title: Thyroid Hormone‐Induced Activation of Notch Signaling is Required for Adult Intestinal Stem Cell Development During Xenopus Laevis Metamorphosis

doi: 10.1002/stem.2544

Figure Lengend Snippet: Correlation of the expression patterns of Notch pathway components with that of a stem/progenitor marker in the metamorphosing intestine. Cross‐sections of the intestine from tadpoles at stages 60 ( A, D ) and 61 ( B, E, G, I ), and stage‐54 tadpoles treated with 10 nM T3 for 3 ( C, F ) and 5 days ( H, J ) were hybridized with antisense Hairy1 ( A‐C ) or Hairy2b ( G, H ) probes. The corresponding serial sections were hybridized with antisense LGR5 probe ( D–F, I, J ) for comparison. Hairy1 is expressed in the adult epithelial stem (AE)/progenitor cells (A, arrowhead) when they first appear as the small islets expressing LGR5 ( D , arrow) at stage 60. These islets grew in size as metamorphosis proceeded and continued to co‐express Hairy1 ( B , arrowheads) and LGR5 ( E , arrows). During T3‐induced metamorphosis, Hairy1 ( C , arrowhead) is also expressed in the AE/progenitor cells expressing LGR5 ( F , arrow) after 3 days of T3 treatment. Some, although not all, cells expressing Hairy2b were in the connective tissue (CT) ( G , arrowheads) underlying the AE/progenitor cells expressing LGR5 ( I , arrows). Hairy2b is also expressed in the CT after 5 days of T3 treatment ( H , arrowheads), again, with some underlying the AE/progenitor cells ( J , arrows). Cross‐sections of the intestine from tadpoles at stage 62 were double‐immunostained with anti‐CK19 to detect the islet of AE/progenitor cells ( K–M , red) and anti‐DLL1 ( K , green), anti‐Jag1 ( L , green), or anti‐Notch1 ( M , green) followed by counterstaining with DAPI ( K–M , blue). DLL1 ( K , arrowheads) and Notch1 ( M , arrowheads) are expressed in the islets (arrows). The cells expressing Jag1 are scattered in both the larval Ep and CT with some just beneath the islet, but not in the islets ( L , arrowheads). The dashed‐lines indicate the boundary of the Ep and the CT. Scale bars = 20 μm. Abbreviations: AE, adult epithelial stem/progenitor cells, CT, connective tissue, Ep, epithelium.

Techniques: Expressing, Marker, Comparison

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