scholarly journals Interplay between a cytosolic and a cell surface carbonic anhydrase in pH homeostasis and acid tolerance ofLeishmania

2017 ◽  
Vol 130 (4) ◽  
pp. 754-766 ◽  
Author(s):  
Dhiman Sankar Pal ◽  
Mazharul Abbasi ◽  
Dipon Kumar Mondal ◽  
Binitha Anu Varghese ◽  
Ritama Paul ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Cell Surface ◽  
Acid Tolerance ◽  
Ph Homeostasis ◽  
A Cell

scholarly journals Thriving at Low pH: Adaptation Mechanisms of Acidophiles

2021 ◽  
Author(s):  
Xianke Chen
Keyword(s):  
Electrical Potential ◽  
Acid Tolerance ◽  
Acid Resistance ◽  
Intelligent Manufacturing ◽  
Membrane Composition ◽  
Ph Homeostasis ◽  
Protein Repair ◽  
A Cell ◽  
Transmembrane Electrical Potential

Acid resistance of acidophiles is the result of long-term co-evolution and natural selection of acidophiles and their natural habitats, and formed a relatively optimal acid-resistance network in acidophiles. The acid tolerance network of acidophiles could be classified into active and passive mechanisms. The active mechanisms mainly include the proton efflux and consumption systems, generation of reversed transmembrane electrical potential, and adjustment of cell membrane composition; the passive mechanisms mainly include the DNA and protein repair systems, chemotaxis and cell motility, and quorum sensing system. The maintenance of pH homeostasis is a cell-wide physiological process that adopt differently adjustment strategies, deployment modules, and integration network depending on the cell’s own potential and its habitat environments. However, acidophiles exhibit obvious strategies and modules similarities on acid resistance because of the long-term evolution. Therefore, a comprehensive understanding of acid tolerance network of acidophiles would be helpful for the intelligent manufacturing and industrial application of acidophiles.

scholarly journals Leukocytes with chromosome Y loss have reduced abundance of the cell surface immunoprotein CD99

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jonas Mattisson ◽  
Marcus Danielsson ◽  
Maria Hammond ◽  
Hanna Davies ◽  
Caroline J. Gallant ◽  
...  
Keyword(s):  
Cell Surface ◽  
Single Cells ◽  
Surface Protein ◽  
Protein Abundance ◽  
Blood Leukocytes ◽  
Chromosome Y ◽  
Increased Risk ◽  
A Cell ◽  
Pseudoautosomal Regions ◽  
Male Specific

AbstractMosaic loss of chromosome Y (LOY) in immune cells is a male-specific mutation associated with increased risk for morbidity and mortality. The CD99 gene, positioned in the pseudoautosomal regions of chromosomes X and Y, encodes a cell surface protein essential for several key properties of leukocytes and immune system functions. Here we used CITE-seq for simultaneous quantification of CD99 derived mRNA and cell surface CD99 protein abundance in relation to LOY in single cells. The abundance of CD99 molecules was lower on the surfaces of LOY cells compared with cells without this aneuploidy in all six types of leukocytes studied, while the abundance of CD proteins encoded by genes located on autosomal chromosomes were independent from LOY. These results connect LOY in single cells with immune related cellular properties at the protein level, providing mechanistic insight regarding disease vulnerability in men affected with mosaic chromosome Y loss in blood leukocytes.

scholarly journals Annexin A2 in Fibrinolysis, Inflammation and Fibrosis

2021 ◽  
Vol 22 (13) ◽  
pp. 6836
Author(s):  
Hana I. Lim ◽  
Katherine A. Hajjar
Keyword(s):  
Cell Surface ◽  
Tissue Injury ◽  
Critical Role ◽  
Annexin A2 ◽  
Hemorrhagic Disease ◽  
Membrane Repair ◽  
Endothelial Cell Surface ◽  
Human Disorders ◽  
A Cell ◽  
Organ Fibrosis

As a cell surface tissue plasminogen activator (tPA)-plasminogen receptor, the annexin A2 (A2) complex facilitates plasmin generation on the endothelial cell surface, and is an established regulator of hemostasis. Whereas A2 is overexpressed in hemorrhagic disease such as acute promyelocytic leukemia, its underexpression or impairment may result in thrombosis, as in antiphospholipid syndrome, venous thromboembolism, or atherosclerosis. Within immune response cells, A2 orchestrates membrane repair, vesicle fusion, and cytoskeletal organization, thus playing a critical role in inflammatory response and tissue injury. Dysregulation of A2 is evident in multiple human disorders, and may contribute to the pathogenesis of various inflammatory disorders. The fibrinolytic system, moreover, is central to wound healing through its ability to remodel the provisional matrix and promote angiogenesis. A2 dysfunction may also promote tissue fibrogenesis and end-organ fibrosis.

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