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Cusabio p icam 1
P Icam 1, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p+icam+1/Rabbit+anti-+Phospho-ICAM1+Polyclonal+Antibody/pm35487888-258-5-10
Average 93 stars, based on 1 article reviews
p icam 1 - by Bioz Stars, 2026-09
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Article Title: ICAM-1 promotes cancer progression by regulating SRC activity as an adapter protein in colorectal cancer.
Article Snippet: The polyclonal antibodies specific for p-ICAM-1 (CSB-PA000547) was purchased from CUSABIO TECHNOLOGY.

Article Title: ICAM-1 promotes cancer progression by regulating SRC activity as an adapter protein in colorectal cancer
Article Snippet: The polyclonal antibodies specific for p-ICAM-1 (CSB-PA000547) was purchased from CUSABIO TECHNOLOGY.



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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 <t>(ICAM-1)</t> area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.
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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 <t>(ICAM-1)</t> area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.
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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 <t>(ICAM-1)</t> area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.
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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 <t>(ICAM-1)</t> area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.
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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 <t>(ICAM-1)</t> area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.
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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 <t>(ICAM-1)</t> area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.
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DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 (ICAM-1) area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.

Journal: iScience

Article Title: DHCR24 inhibitor SH42 increases desmosterol without preventing atherosclerosis development in mice

doi: 10.1016/j.isci.2024.109830

Figure Lengend Snippet: DHCR24 inhibitor SH42 decreases circulating non-classical monocytes without affecting atherosclerosis development in LDL receptor knockout mice After 13 weeks of treatment, mice were killed and the relative number of blood monocytes (A) and their subsets (B) were quantified. Hearts were collected, the aortic root valve areas were stained with hematoxylin-phloxine-saffron (HPS), and representative pictures are shown (C). The atherosclerotic lesion area (D) was determined and lesions were categorized according to lesion severity (E). Intercellular adhesion molecule 1 (ICAM-1) area (G) in lesions was stained using an anti-ICAM-1 antibody. Representative pictures are shown (F). The smooth muscle cell (I), collagen (J) and macrophage (K) areas of the lesions were determined by staining aortic root lesions with an anti-α-actin antibody, Sirius Red and anti-MAC3 antibody, respectively. Representative pictures are shown (H). The stability index (smooth muscle cell area and collagen area/macrophage area of the lesions) was calculated (L). CM, classical monocyte; IM, intermediate monocyte; NCM, nonclassical monocyte. Data are shown as mean ± SEM. n = 13–15 mice per group. Data were analyzed by unpaired two-tailed Student’s t test. ∗ p < 0.05, ∗∗∗ p < 0.001.

Article Snippet: In experiment 3, Intercellular adhesion molecule 1 (ICAM-1) area was stained using an anti-ICAM-1 antibody (Sino Biological, USA) and a secondary antibody EnVision System-HRP Labeled Polymer (Dako, Denmark) that was visualized by Liquid DAB + Substrate Chromogen System (Dako, Denmark).

Techniques: Knock-Out, Staining, Two Tailed Test