anti pkn2 mab Search Results


90
Becton Dickinson α-pkn1
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Cell Signaling Technology Inc p pdk1
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Cell Signaling Technology Inc anti gapdh
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Cell Signaling Technology Inc e cadherin
A) <t>E-cadherin</t> staining of adherens junctions in PKN2 knockout CRISPR cells. B-E) Loss of ZO1-positive tight junctions (A, D) and gain in PKN2 expression (C, D, E) following overexpression of a kinase-dead (KD) PKN2 in the inducible DLD1 cell line (iDLD1). Statistical significance was determined using an unpaired, two-tailed t-test (n=5). F-I) Change in average junction length per cell (F, G) and gain in PKN2 expression (G, H, I) following overexpression of wild-type PKN2. Statistical significance was determined using an unpaired, two-tailed t-test (n=3). J-K) No statistically significant difference in CellTitre Glo intensity between CRISPR control and PKN2 KO gRNA lines following PKN2 KO, 4mM EGTA treatment (J) or 50mg/ml DSS (K). Statistical significance was determined using an unpaired, two-tailed t-test (J: n=4, K: n=5).
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Cell Signaling Technology Inc anti phospho thr
A) <t>E-cadherin</t> staining of adherens junctions in PKN2 knockout CRISPR cells. B-E) Loss of ZO1-positive tight junctions (A, D) and gain in PKN2 expression (C, D, E) following overexpression of a kinase-dead (KD) PKN2 in the inducible DLD1 cell line (iDLD1). Statistical significance was determined using an unpaired, two-tailed t-test (n=5). F-I) Change in average junction length per cell (F, G) and gain in PKN2 expression (G, H, I) following overexpression of wild-type PKN2. Statistical significance was determined using an unpaired, two-tailed t-test (n=3). J-K) No statistically significant difference in CellTitre Glo intensity between CRISPR control and PKN2 KO gRNA lines following PKN2 KO, 4mM EGTA treatment (J) or 50mg/ml DSS (K). Statistical significance was determined using an unpaired, two-tailed t-test (J: n=4, K: n=5).
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Cell Signaling Technology Inc rhoa
A) <t>E-cadherin</t> staining of adherens junctions in PKN2 knockout CRISPR cells. B-E) Loss of ZO1-positive tight junctions (A, D) and gain in PKN2 expression (C, D, E) following overexpression of a kinase-dead (KD) PKN2 in the inducible DLD1 cell line (iDLD1). Statistical significance was determined using an unpaired, two-tailed t-test (n=5). F-I) Change in average junction length per cell (F, G) and gain in PKN2 expression (G, H, I) following overexpression of wild-type PKN2. Statistical significance was determined using an unpaired, two-tailed t-test (n=3). J-K) No statistically significant difference in CellTitre Glo intensity between CRISPR control and PKN2 KO gRNA lines following PKN2 KO, 4mM EGTA treatment (J) or 50mg/ml DSS (K). Statistical significance was determined using an unpaired, two-tailed t-test (J: n=4, K: n=5).
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Cell Signaling Technology Inc antibodies to cd45
A) <t>E-cadherin</t> staining of adherens junctions in PKN2 knockout CRISPR cells. B-E) Loss of ZO1-positive tight junctions (A, D) and gain in PKN2 expression (C, D, E) following overexpression of a kinase-dead (KD) PKN2 in the inducible DLD1 cell line (iDLD1). Statistical significance was determined using an unpaired, two-tailed t-test (n=5). F-I) Change in average junction length per cell (F, G) and gain in PKN2 expression (G, H, I) following overexpression of wild-type PKN2. Statistical significance was determined using an unpaired, two-tailed t-test (n=3). J-K) No statistically significant difference in CellTitre Glo intensity between CRISPR control and PKN2 KO gRNA lines following PKN2 KO, 4mM EGTA treatment (J) or 50mg/ml DSS (K). Statistical significance was determined using an unpaired, two-tailed t-test (J: n=4, K: n=5).
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Image Search Results


A) E-cadherin staining of adherens junctions in PKN2 knockout CRISPR cells. B-E) Loss of ZO1-positive tight junctions (A, D) and gain in PKN2 expression (C, D, E) following overexpression of a kinase-dead (KD) PKN2 in the inducible DLD1 cell line (iDLD1). Statistical significance was determined using an unpaired, two-tailed t-test (n=5). F-I) Change in average junction length per cell (F, G) and gain in PKN2 expression (G, H, I) following overexpression of wild-type PKN2. Statistical significance was determined using an unpaired, two-tailed t-test (n=3). J-K) No statistically significant difference in CellTitre Glo intensity between CRISPR control and PKN2 KO gRNA lines following PKN2 KO, 4mM EGTA treatment (J) or 50mg/ml DSS (K). Statistical significance was determined using an unpaired, two-tailed t-test (J: n=4, K: n=5).

Journal: bioRxiv

Article Title: PKN2 regulates cell-junctions to limit colitis and colon tumour formation

doi: 10.64898/2025.12.15.694339

Figure Lengend Snippet: A) E-cadherin staining of adherens junctions in PKN2 knockout CRISPR cells. B-E) Loss of ZO1-positive tight junctions (A, D) and gain in PKN2 expression (C, D, E) following overexpression of a kinase-dead (KD) PKN2 in the inducible DLD1 cell line (iDLD1). Statistical significance was determined using an unpaired, two-tailed t-test (n=5). F-I) Change in average junction length per cell (F, G) and gain in PKN2 expression (G, H, I) following overexpression of wild-type PKN2. Statistical significance was determined using an unpaired, two-tailed t-test (n=3). J-K) No statistically significant difference in CellTitre Glo intensity between CRISPR control and PKN2 KO gRNA lines following PKN2 KO, 4mM EGTA treatment (J) or 50mg/ml DSS (K). Statistical significance was determined using an unpaired, two-tailed t-test (J: n=4, K: n=5).

Article Snippet: Primary antibodies: PKN2 (R&D, MAB5686), ZO-1 (Invitrogen, 61-7300), E-cadherin (Cell Signaling Technology, 3195T), Phalloidin (Invitrogen, A22283).

Techniques: Staining, Knock-Out, CRISPR, Expressing, Over Expression, Two Tailed Test, Control