mil 13 (Cell Signaling Technology Inc)
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90
Structured Review
Cell Signaling Technology Inc
mil 13
Mil 13, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mil+13/Mouse+Interleukin-13/pm39643140-143-20-22
Average 90 stars, based on 7 article reviews
Mil 13, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mil+13/Mouse+Interleukin-13/pm39643140-143-20-22
Average 90 stars, based on 7 article reviews
mil 13 - by Bioz Stars,
2026-10
90/100 stars
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Incubation:Article Title: Bruton tyrosine kinase promotes wound healing after myocardial infarction by inhibiting the transcription of u-PA. Article Snippet: Backgrounds: Bruton tyrosine kinase (BTK), which is highly expressed in immune cells, plays a critical role in regulating the function of macrophages.. A growing body of evidence has demonstrated that the accumulation of macrophages in cardiac tissue after myocardial infarction (MI) significantly affects wound healing and ventricular remodeling during the early phase of repair after MI.. However, the role of BTK in cardiac repair post-MI, especially in macrophage-mediated repair, remains unclear. Cell Culture:Article Title: Bruton tyrosine kinase promotes wound healing after myocardial infarction by inhibiting the transcription of u-PA. Article Snippet: Backgrounds: Bruton tyrosine kinase (BTK), which is highly expressed in immune cells, plays a critical role in regulating the function of macrophages.. A growing body of evidence has demonstrated that the accumulation of macrophages in cardiac tissue after myocardial infarction (MI) significantly affects wound healing and ventricular remodeling during the early phase of repair after MI.. However, the role of BTK in cardiac repair post-MI, especially in macrophage-mediated repair, remains unclear. |