Altered Protein Abundance and Localization Inferred from Sites of Alternative Modification by Ubiquitin and SUMO

2021 ◽  
Vol 433 (21) ◽  
pp. 167219
Author(s):  
Adi Ulman ◽  
Tal Levin ◽  
Bareket Dassa ◽  
Aaron Javitt ◽  
Assaf Kacen ◽  
...  
Keyword(s):  
Protein Abundance ◽  
Altered Protein

scholarly journals Short-term high-glucose treatment decreased abundance of Orai1 protein through posttranslational mechanisms in rat mesangial cells

2018 ◽  
Vol 314 (5) ◽  
pp. F855-F863 ◽  
Author(s):  
Hui Jiang ◽  
Shubiao Zou ◽  
Sarika Chaudhari ◽  
Rong Ma
Keyword(s):  
High Glucose ◽  
Mesangial Cells ◽  
Protein Synthesis Inhibitor ◽  
Protein Abundance ◽  
Oxygen Species ◽  
Short Term ◽  
Synthesis Inhibitor ◽  
Altered Protein ◽  
Short Period ◽  
Ubiquitin Proteasome

The short-term effect of high-glucose (HG) treatment on store-operated Ca2+ entry in mesangial cells (MCs) is not well-known. The aim of the present study was to determine whether and how HG treatment for a short period altered protein abundance of Orai1, the channel mediating store-operated Ca2+ entry in MCs. Rat and human MCs were exposed to HG (25 mM) for 2, 4, 8, and 24 h, and the abundance of Orai1 protein was significantly decreased at the time points of 8 and 16 h. Consistently, HG treatment for 8 h significantly reduced store-operated Ca2+ entry in rat MCs. However, HG treatment for the same time periods did not alter the levels of Orai1 transcript. Cycloheximide, a protein synthesis inhibitor, did not affect the HG-induced decrease of Orai1 protein, suggesting a posttranslational mechanism was involved. However, the HG effect on Orai1 protein was significantly attenuated by MG132 (a ubiquitin-proteasome inhibitor) and NH4Cl (a lysosomal pathway inhibitor). Furthermore, HG treatment for 8 h stimulated ubiquitination of Orai1 protein. We further found that polyethylene glycol-catalase, an antioxidant, significantly blunted the HG-induced reduction of Orai1 protein. In support of involvement of reactive oxygen species in the HG effects, hydrogen peroxide (H2O2) itself significantly decreased abundance of Orai1 protein and increased the level of ubiquitinated Orai1. Taken together, these results suggest that a short-term HG treatment decreased abundance of Orai1 protein in MCs by promoting the protein degradation through the ubiquitination-proteasome and –lysosome mechanisms. This HG-stimulated posttranslational mechanism was mediated by H2O2.

Proteomic analysis of porcine endometrial tissue during peri-implantation period reveals altered protein abundance

2015 ◽  
Vol 125 ◽  
pp. 76-88 ◽  
Author(s):  
Beenu Moza Jalali ◽  
Marek Bogacki ◽  
Mariola Dietrich ◽  
Pawel Likszo ◽  
Marta Wasielak
Keyword(s):  
Proteomic Analysis ◽  
Endometrial Tissue ◽  
Protein Abundance ◽  
Altered Protein ◽  
Implantation Period

Head Size and DNA Content in Bacteriophage T4

1972 ◽  
Vol 30 ◽  
pp. 200-201
Author(s):  
Fred Eiserling ◽  
A. H. Doermann ◽  
Linde Boehner
Keyword(s):  
Electron Microscopy ◽  
Dna Content ◽  
Bacteriophage T4 ◽  
Head Size ◽  
Virus Particles ◽  
Altered Protein ◽  
A Cell ◽  
Bacterial Viruses ◽  
A Site ◽  
Protein Shell

The control of form or shape inheritance can be approached by studying the morphogenesis of bacterial viruses. Shape variants of bacteriophage T4 with altered protein shell (capsid) size and nucleic acid (DNA) content have been found by electron microscopy, and a mutant (E920g in gene 66) controlling head size has been described. This mutant produces short-headed particles which contain 2/3 the normal DNA content and which are non-viable when only one particle infects a cell (Fig. 1).We report here the isolation of a new mutant (191c) which also appears to be in gene 66 but at a site distinct from E920g. The most striking phenotype of the mutant is the production of about 10% of the phage yield as “giant” virus particles, from 3 to 8 times longer than normal phage (Fig. 2).

1047: Rock-II Protein Abundance is Increased in Diabetic and Cavernous Nerve Injured Penes

2005 ◽  
Vol 173 (4S) ◽  
pp. 284-284
Author(s):  
Carol A. Podlasek ◽  
Douglas Wood ◽  
Yi Tang ◽  
Kevin E. McKenna ◽  
Kevin T. McVary
Keyword(s):  
Protein Abundance ◽  
Cavernous Nerve

Altered protein synthesis during in situ oat leaf senescence

1990 ◽  
Vol 80 (4) ◽  
pp. 619-623 ◽  
Author(s):  
Louise Lalonde ◽  
Rajinder S. Dhindsa
Keyword(s):  
Protein Synthesis ◽  
Leaf Senescence ◽  
Altered Protein

Programming Water Transporter Aquaporin Z by Lipid Composition-Altered Protein Dynamics

2018 ◽  
Author(s):  
Xin-Shan Lim ◽  
Xin-Xiang Lim ◽  
Lili Wang ◽  
Hu Zhou ◽  
Ganesh S. Anand ◽  
...  
Keyword(s):  
Protein Dynamics ◽  
Lipid Composition ◽  
Altered Protein ◽  
Aquaporin Z

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.

Sex differences in prenatal programming of hypertension by dexamethasone

2021 ◽  
pp. 153537022110032
Author(s):  
Issa Alhamoud ◽  
Susan K Legan ◽  
Jyothsna Gattineni ◽  
Michel Baum
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Female Offspring ◽  
Male Offspring ◽  
Thick Ascending Limb ◽  
Protein Abundance ◽  
Female Rat ◽  
Prenatal Programming ◽  
Transporter Protein ◽  
Renal Tubular

Prenatal dexamethasone has been shown to increase blood pressure in male offspring but the mechanism for the increase in blood pressure is unclear. The present study examined if prenatal programming by maternal injection of dexamethasone on days 15 and 16 of gestation affected the blood pressure comparably in female and male offspring. Our hypothesis was that males would be affected by prenatal dexamethasone to a greater extent than females and that either an increase in renal tubular transporter abundance or an increase in renin or aldosterone system would be associated with hypertension with prenatal programming. Prenatal dexamethasone increased blood pressure at two months and six months of age and resulted in proteinuria and albuminuria at six months in male but not female rat offspring. There was no effect of prenatal dexamethasone on blood pressure and proteinuria at one month in male and in female offspring. While prenatal dexamethasone increased male renal thick ascending limb sodium potassium two chloride cotransporter protein abundance at two months, prenatal dexamethasone on days 15 and 16 of gestation did not affect transporter abundance in males at other ages, nor did it affect proximal tubule sodium/hydrogen exchanger or distal convoluted tubule sodium chloride cotransporter protein abundance at any age. There was no difference in systemic renin or aldosterone in the prenatal dexamethasone group compared to same sex controls. In conclusion, male but not female offspring have an increase in blood pressure and urinary protein excretion with prenatal dexamethasone. The increase in blood pressure with prenatal programming was not associated with a consistent increase in renal tubular transporter protein abundance, nor plasma renin activity and serum aldosterone.

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