scholarly journals The role of inositol 1,4,5-trisphosphate in mobilizing calcium from intracellular stores in the salivary glands of Amblyomma americanum (L.)

1990 ◽  
Vol 20 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Craig W. Roddy ◽  
Janis L. McSwain ◽  
Katherine M. Kocan ◽  
Richard C. Essenberg ◽  
John R. Sauer
Keyword(s):  
Salivary Glands ◽  
Amblyomma Americanum ◽  
Inositol 1,4,5 Trisphosphate

scholarly journals Alpha-Gal Syndrome: Involvement of Amblyomma americanum α-D-Galactosidase and β-1,4 Galactosyltransferase Enzymes in α-Gal Metabolism

2021 ◽  
Vol 11 ◽  
Author(s):  
Surendra Raj Sharma ◽  
Gary Crispell ◽  
Ahmed Mohamed ◽  
Cameron Cox ◽  
Joshua Lange ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Basophil Activation Test ◽  
Amblyomma Americanum ◽  
Delayed Type Hypersensitivity ◽  
Galactose Metabolism ◽  
Lone Star Tick ◽  
Intrinsic Factors ◽  
Significant Difference ◽  
Ige Mediated

Alpha-Gal Syndrome (AGS) is an IgE-mediated delayed-type hypersensitivity reaction to the oligosaccharide galactose-α-1, 3-galactose (α-gal) injected into humans from the lone-star tick (Amblyomma americanum) bite. Indeed, α-gal is discovered in salivary glands of lone-star tick; however, the tick’s specific intrinsic factors involved in endogenous α-gal production and presentation to host during hematophagy are poorly understood. This study aimed to investigate the functional role of two tick enzymes, α-D-galactosidase (ADGal) and β-1,4 galactosyltransferases (β-1,4GalT), in endogenous α-gal production, carbohydrate metabolism, and N-glycan profile in lone-star tick. The ADGal enzyme cleaves terminal α-galactose moieties from glycoproteins and glycolipids, whereas β-1,4GalT transfers α-galactose to a β1,4 terminal linkage acceptor sugars—GlcNAc, Glc, and Xyl—in various processes of glycoconjugate synthesis. An RNA interference approach was utilized to silence ADGal and β-1,4GalT in Am. americanum to examine their function in α-gal metabolism in tick and AGS onset. Silencing of ADGal led to the significant downregulation of genes involved in galactose metabolism and transport in Am. americanum. Immunoblot and N-glycan analysis of the Am. americanum salivary glands showed a significant reduction in α-gal levels in silenced tissues. However, there was no significant difference in the level of α-gal in β-1,4GalT-silenced tick salivary glands. A basophil-activation test showed a decrease in the frequency of activated basophil by ADGal-silenced salivary glands. These results provide an insight into the roles of ADGal and β-1,4GalT in α-gal production and presentation in ticks and the probable involvement in the onset of AGS.

scholarly journals Alpha-Gal Syndrome: Involvement of Amblyomma americanum α-D-galactosidase and α-1,4 Galactosyltransferase enzymes in α-gal metabolism

2021 ◽  
Author(s):  
Surendra Raj Sharma ◽  
Gary Crispell ◽  
Ahmed Mohamed ◽  
Cameron Cox ◽  
Joshua Lange ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Functional Characterization ◽  
Basophil Activation Test ◽  
Amblyomma Americanum ◽  
Delayed Type Hypersensitivity ◽  
Galactose Metabolism ◽  
Significant Difference ◽  
Ige Mediated

AbstractAlpha-Gal Syndrome (AGS) is an IgE-mediated delayed-type hypersensitivity reaction to the oligosaccharide galactose-⍰-1,3-galactose (α-gal) injected into humans from the lone star tick (Amblyomma americanum) bite. This study aims at the functional characterization of two tick enzymes, α-D-galactosidase (ADGal) and α-1,4 galactosyltransferase (β-1,4GalT) in α-gal metabolism. The ADGal enzyme cleaves terminal α-galactose moieties from glycoproteins and glycolipids, whereas β-1,4GalT transfers α-galactose to a β1,4 terminal linkage acceptor sugars: GlcNAc, Glc, and Xyl in various processes of glycoconjugate synthesis. An RNA interference approach was utilized to silence ADGal and β-1,4GalT in Am. americanum to examine their functional role in α-gal metabolism and AGS onset. Silencing of ADGal led to the significant down regulation of genes involved in galactose metabolism and transport in Am. americanum. Immunoblot and N-glycan analysis of the Am. americanum salivary glands showed a significant reduction in ⍰-gal levels in silenced tissues. However, there was no significant difference in the level of ⍰-gal in β-1,4GalT silenced tick salivary glands. A basophil-activation test showed a decrease in the frequency of activated basophil by ADGal silenced salivary glands. These results provide an insight into the role of α-D galactosidase & β-1,4GalT in tick biology and the probable involvement in the onset of AGS.

scholarly journals Inhibition of Aurora Kinase B activity disrupts development and differentiation of salivary glands

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer K. Shaalan ◽  
Tathyane H. N. Teshima ◽  
Abigail S. Tucker ◽  
Gordon B. Proctor
Keyword(s):  
Cell Cycle ◽  
Embryonic Development ◽  
Salivary Glands ◽  
Aurora Kinase ◽  
Serine Threonine Kinase ◽  
Aurora Kinase B ◽  
Development And Differentiation ◽  
Differentiation Marker ◽  
Key Events

AbstractLittle is known about the key molecules that regulate cell division during organogenesis. Here we determine the role of the cell cycle promoter aurora kinase B (AURKB) during development, using embryonic salivary glands (E-SGs) as a model. AURKB is a serine/threonine kinase that regulates key events in mitosis, which makes it an attractive target for tailored anticancer therapy. Many reports have elaborated on the role of AURKB in neoplasia and cancer; however, no previous study has shown its role during organ development. Our previous experiments have highlighted the essential requirement for AURKB during adult exocrine regeneration. To investigate if AURKB is similarly required for progression during embryonic development, we pharmacologically inhibited AURKB in developing submandibular glands (SMGs) at embryonic day (E)13.5 and E16.5, using the highly potent and selective drug Barasertib. Inhibition of AURKB interfered with the expansion of the embryonic buds. Interestingly, this effect on SMG development was also seen when the mature explants (E16.5) were incubated for 24 h with another cell cycle inhibitor Aphidicolin. Barasertib prompted apoptosis, DNA damage and senescence, the markers of which (cleaved caspase 3, γH2AX, SA-βgal and p21, respectively), were predominantly seen in the developing buds. In addition to a reduction in cell cycling and proliferation of the epithelial cells in response to AURKB inhibition, Barasertib treatment led to an excessive generation of reactive oxygen species (ROS) that resulted in downregulation of the acinar differentiation marker Mist1. Importantly, inhibition of ROS was able to rescue this loss of identity, with Mist1 expression maintained despite loss of AURKB. Together, these data identify AURKB as a key molecule in supporting embryonic development and differentiation, while inhibiting senescence-inducing signals during organogenesis.

scholarly journals Unraveling the role of polycystin-2/inositol 1,4,5-trisphosphate receptor interaction in Ca2+signaling

2010 ◽  
Vol 3 (6) ◽  
pp. 530-532 ◽  
Author(s):  
Eva Sammels ◽  
Benoit Devogelaere ◽  
Djalila Mekahli ◽  
Geert Bultyncki ◽  
Ludwig Missiaen ◽  
...  
Keyword(s):  
Receptor Interaction ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

Antigenic variation in its biological context

1984 ◽  
Vol 307 (1131) ◽  
pp. 27-40 ◽  
Keyword(s):  
Salivary Glands ◽  
Antigenic Variation ◽  
Tsetse Fly ◽  
Mammalian Host ◽  
Full Understanding ◽  
Anamnestic Response ◽  
Insect Midgut ◽  
The Relationship ◽  
Biological Context

The biology of antigenic variation is discussed, and the problems that must be solved to provide a full understanding of antigenic variation are considered. These are (i) the induction of v.s.g. synthesis in the salivary glands of the tsetse fly; (ii) the nature of the restriction on v.s.g. genes that allows only some of them to be expressed in the salivary glands; (iii) the nature of ‘predominance’ in v.s.g. expression in the mammalian host, and the mechanism by which it operates; (iv) the repression of v.s.g. synthesis in the insect midgut; (v) the anamnestic response that produces expression of the ingested variant in the first patent parasitaemia in the mammalian host; (vi) the mechanism by which only one v.s.g. gene at a time is expressed; (vii) the relationship if any ofv.s.g. structure to v.s.g.-associated differences in growth rate and host range; (viii) the role of v.s.g. release within the life cycle and to pathogenesis.

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