کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8293306 | 1536744 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Protein tyrosine kinase A modulates intracellular survival of mycobacteria through Galectin 3
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Mycobacterium tuberculosis (MTB) is a successful pathogen which increases persistence inside the host macrophage by subverting its defence mechanism. Mycobacteria regulate the pathogenesis and intracellular survival by controlling its interaction with host protein(s). Galectin 3 is a member of the β-galactoside binding gene family which is involved in several biological functions. In the present study, we have expressed the mycobacterial protein tyrosine kinase (PtkA) in the cytosol of host macrophages through a eukaryotic promoter vector and found that it down-regulates Galectin 3. Infection by ptkA knocked-out (KO) mycobacterial strain shows increased level of Galectin 3 in the cytosol of macrophages. PtkA regulates Galectin 3 level and stimulates host macrophage through MEK-JNK-cJUN pathway and initiates early apoptosis in H37Ra infected macrophage. The ptkA KO strain showed decreased progression of apoptosis confirming Galectin 3 as anti-apoptotic molecule. The intracellular survival was also found to be impaired in the mice infected with ptkA KO mycobacteria. The hypothesis was also confirmed by looking at the intracellular survival of mycobacteria in Galectin 3 silenced macrophages. The overall findings suggest the significance of Galectin 3 and PtkA interaction in intracellular persistence of mycobacteria.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 498, Issue 4, 15 April 2018, Pages 884-890
Journal: Biochemical and Biophysical Research Communications - Volume 498, Issue 4, 15 April 2018, Pages 884-890
نویسندگان
Swati Jaiswal, Kishore K. Srivastava,