scholarly journals Relationship of Ribulose-1,5-bisphosphate Carboxylase-Oxygenase Specific Activity to Subunit Composition

1980 ◽  
Vol 65 (1) ◽  
pp. 69-73 ◽  
Author(s):  
Patsy R. Rhodes ◽  
Shain-Dow Kung ◽  
Thomas V. Marsho
1981 ◽  
Vol 2 (4) ◽  
pp. 235-242 ◽  
Author(s):  
James T. Bahr ◽  
Sarjit Johal ◽  
Malcolm Capel ◽  
Don P. Bourque

Bibliosphere ◽  
2016 ◽  
pp. 107-111
Author(s):  
L. A. Mosunova

Editorial art is treated as realization of the relationship of artistic-aesthetic and intellectual-speech activities. This specific activity is formed under certain conditions of learning editing, where it becomes a form of self-expression, conscience of students, means of their self-development. The principles of this training, the main one of which is the editing structural-functional organization in situation of joint productive activity, are described.


1988 ◽  
Vol 255 (1) ◽  
pp. E94-E98 ◽  
Author(s):  
S. L. Lehman ◽  
W. C. Stanley

When a substrate appears in and disappears from an unmeasured (tissue) compartment, the proper sites for tracer infusion and sampling to measure tracee turnover become controversial. We analyze a three-compartment model representing arterial blood, tissue, and venous blood. The desired quantity, tracee turnover, is the ratio of the steady-state infusion rate to tissue specific activity. However, specific activity in the tissue compartment is unknown. We assume infusion of tracer into the arterial pool at a constant rate and consider sampling of specific activity of either blood compartment in the steady state. We obtain estimates of tissue specific activity from measurement of concentrations of tracer and tracee in blood samples in two extreme cases. In case I, tracee is assumed to appear in the venous compartment but to disappear from the tissue pool. Then tissue specific activity is equal to arterial specific activity. In case II, both appearance and disappearance are from the tissue pool. Tissue specific activity is then less than arterial or venous specific activity. We give formulas for the difference in each case. We discuss the relationship of our models to actual tracer experiments and define physiological locations for our three compartments. Appearance of substrates is probably intermediate between our extreme cases. A numerical estimate of turnover for the substrate lactate in resting humans reveals an error bound of approximately 30%. We discuss sites of infusion and sampling consistent with our model, the effects of relaxing some of our modeling constraints, and experimental necessities for getting beyond the steady state.


1987 ◽  
Vol 253 (2) ◽  
pp. E173-E178 ◽  
Author(s):  
D. K. Layman ◽  
R. R. Wolfe

The optimal arterial or venous sites for infusion and sampling during isotopic tracer studies have not been established. This study determined the relationship of plasma and tissue enrichment (E) when isotopes were infused in an artery and sampled from a vein (av mode) or infused in a vein and sampled from an artery (va mode). Adult dogs were given primed constant infusions of [3-13C]lactate, [1-13C]leucine, and 14C-labeled bicarbonate. Simultaneous samples were drawn from the vena cava, aortic arch, and breath. Tissue samples were removed from skeletal muscle, liver, kidney, and gut. Breath samples were analyzed for 14CO2 by liquid scintillation counting and plasma isotopic enrichments of [13C]lactate, [13C]leucine, and alpha-[13C]ketoisocaproate (KIC) were determined by gas chromatography-mass spectrometry. By using the va mode, the plasma E for lactate and leucine were 30-40% above tissue E. The av mode provided an accurate reflection of tissue E for lactate, which equilibrates rapidly with tissues, and a reasonable estimate for leucine, which exchanges more slowly. The isotopic enrichment of plasma KIC more directly reflected tissue leucine E than did plasma leucine E, and KIC enrichment was insensitive to sampling site. We also evaluated theoretically a circulatory model that predicts venous isotopic enrichments when the va mode is used. We conclude that the av mode is optimal but that the problems arising from use of the va mode can be overcome by use of a metabolic product (i.e., KIC) or by calculation of venous specific activity with our circulatory mode.


Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 241-241
Author(s):  
Jian Xu ◽  
Zhen Shao ◽  
Dan Li ◽  
Huafeng Xie ◽  
Woojin Kim ◽  
...  

Abstract The epigenetic machinery plays crucial roles in hematopoiesis, and its deregulation drives the pathogenesis of blood disorders. Polycomb Repressive Complex 2 (PRC2) is a major class of epigenetic repressor that catalyzes the di/tri-methylation of histone H3 lysine 27 (or H3K27me2/3). The canonical PRC2 complex consists of EED, SUZ12, and the histone methyltransferase EZH2. The functions of PRC2 in hematopoiesis remain elusive due in large to the existence of two highly related enzymatic subunits EZH1 and EZH2. While amplification or overexpression of PRC2 proteins is common in many cancers, inactivating mutation in PRC2 is frequently found in hematopoietic malignancies, indicating that PRC2 can be oncogenic or tumor suppressive in different cellular contexts. In light of recent efforts to therapeutically target EZH2 enzyme activities or canonical EZH2-PRC2 functions in various hematopoietic malignancies, it will be critical to fully assess the context-specific activity of this epigenetic complex in normal and malignant developmental processes. The molecular mechanisms by which PRC2 regulates normal and neoplastic hematopoiesis is unclear, as are the non-redundant effects of canonical versus non-canonical PRC2 functions, which are mediated by EZH1 or EZH2 independent of H3K27me2/3. In this study, we demonstrate that the PRC2 enzymatic subunits EZH1 and EZH2 undergo an expression switch during hematopoiesis. EZH2 is highly expressed in primary human CD34+ hematopoietic stem/progenitor (HSPC) cells and progressively downregulated during erythroid and lymphoid specification, whereas EZH1 is significantly upregulated during differentiation. We next examined the in vivo stoichiometry of the PRC2 complexes by quantitative proteomics and revealed the existence of an EZH1-SUZ12 sub-complex lacking EED subunit in human erythroid cells. Through genome scale chromatin occupancy (by ChIP-seq) and transcriptional profiling (by RNA-seq) analyses, we provide evidence that EZH1 together with SUZ12 form a non-canonical PRC2 complex, occupy active chromatin domains marked by H3K4me3 and H3K27me1, and positively regulate gene expression. Furthermore, loss of EZH2 expression leads to global repositioning of EZH1 chromatin occupancy to EZH2 targets, and EZH1 complements EZH2 loss within canonical PRC2 target genes. To elucidate the regulatory networks underlying the developmental control of EZH1/2 switch, we profiled the histone modifications and chromatin accessibility surrounding the EZH1 gene in both CD34+ HSPCs and committed erythroid cells. We identified and characterized an erythroid-selective enhancer element that is indispensable for the transcriptional activation of EZH1. Loss of function analysis using CRISPR/cas9-mediated enhancer deletion results in markedly decrease in EZH1 expression in human erythroid cells. Moreover, a switch from GATA2 to GATA1 expression controls the developmental EZH1/2 switch by differential association with distinct EZH1 enhancers during erythroid differentiation. Thus, the lineage- and developmental stage-specific regulation of PRC2 subunit composition leads to a switch from canonical silencing to non-canonical PRC2 functions. Our study also establishes a molecular link between the switch of master lineage regulators and developmental control of PRC2 composition, providing a means to coordinate linage-specific transcription and accompanying changes in the epigenetic landscape during blood stem cell specification. Disclosures No relevant conflicts of interest to declare.


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