Role of adenovirus E1B proteins in transformation: altered organization of intermediate filaments in transformed cells that express the 19-kilodalton protein

1990 ◽  
Vol 10 (1) ◽  
pp. 120-130
Author(s):  
E White ◽  
R Cipriani
Keyword(s):  
Intermediate Filaments ◽  
Expression Vectors ◽  
Transformed Cells ◽  
Gene Products ◽  
Primary Cells ◽  
Subsequent Growth ◽  
Protein Functions ◽  
Adenovirus E1b

Cooperation of the nuclear oncogene E1A with the E1B oncogene is required for transformation of primary cells. Expression vectors were constructed to produce the 19-kilodalton (19K) and 55K E1B proteins under the direction of heterologous promoters in order to investigate the role of individual E1B proteins in transformation. Coexpression of E1A and either the 19K or 55K E1B gene products was sufficient for the formation of transformed foci in primary rat cells at half the frequency of an intact E1B gene, suggesting that the 19K and 55K proteins function via independent pathways in transformation. Furthermore, the effects of Ha-ras and the E1B 19K gene product were additive when cotransfected with E1A, suggesting that the 19K protein functions in transformation by a mechanism independent from that of ras as well. Although expression of E1A and either E1B protein was sufficient for the subsequent growth of cells in long-term culture, the 19K protein was required to support growth in semisolid media. As the 19K protein has been shown to associate with and disrupt intermediate filaments (IFs) when transiently expressed with plasmid vectors (E. White and R. Cipriani, Proc. Natl. Acad. Sci. USA, 86:9886-9890, 1989), the organization of IFs in transformed cells was investigated. Primary rat cells transformed by plasmids encoding E1A plus the E1B 19K protein showed gross perturbations of IFs, whereas cell lines transformed by plasmids encoding E1A plus the E1B 55K protein or E1A plus Ha-ras did not. These results suggest that an intact IF cytoskeleton may inhibit anchorage-independent growth and that the E1B 19K protein can overcome this inhibition by disrupting the IF cytoskeleton.

scholarly journals Role of adenovirus E1B proteins in transformation: altered organization of intermediate filaments in transformed cells that express the 19-kilodalton protein.

1990 ◽  
Vol 10 (1) ◽  
pp. 120-130 ◽  
Author(s):  
E White ◽  
R Cipriani
Keyword(s):  
Intermediate Filaments ◽  
Expression Vectors ◽  
Transformed Cells ◽  
Gene Products ◽  
Primary Cells ◽  
Subsequent Growth ◽  
Protein Functions ◽  
Adenovirus E1b

Cooperation of the nuclear oncogene E1A with the E1B oncogene is required for transformation of primary cells. Expression vectors were constructed to produce the 19-kilodalton (19K) and 55K E1B proteins under the direction of heterologous promoters in order to investigate the role of individual E1B proteins in transformation. Coexpression of E1A and either the 19K or 55K E1B gene products was sufficient for the formation of transformed foci in primary rat cells at half the frequency of an intact E1B gene, suggesting that the 19K and 55K proteins function via independent pathways in transformation. Furthermore, the effects of Ha-ras and the E1B 19K gene product were additive when cotransfected with E1A, suggesting that the 19K protein functions in transformation by a mechanism independent from that of ras as well. Although expression of E1A and either E1B protein was sufficient for the subsequent growth of cells in long-term culture, the 19K protein was required to support growth in semisolid media. As the 19K protein has been shown to associate with and disrupt intermediate filaments (IFs) when transiently expressed with plasmid vectors (E. White and R. Cipriani, Proc. Natl. Acad. Sci. USA, 86:9886-9890, 1989), the organization of IFs in transformed cells was investigated. Primary rat cells transformed by plasmids encoding E1A plus the E1B 19K protein showed gross perturbations of IFs, whereas cell lines transformed by plasmids encoding E1A plus the E1B 55K protein or E1A plus Ha-ras did not. These results suggest that an intact IF cytoskeleton may inhibit anchorage-independent growth and that the E1B 19K protein can overcome this inhibition by disrupting the IF cytoskeleton.

scholarly journals Role of STE genes in the mating factor signaling pathway mediated by GPA1 in Saccharomyces cerevisiae.

1988 ◽  
Vol 8 (9) ◽  
pp. 3777-3783 ◽  
Author(s):  
N Nakayama ◽  
Y Kaziro ◽  
K Arai ◽  
K Matsumoto
Keyword(s):  
Steady State ◽  
Signaling Pathway ◽  
State Level ◽  
G1 Arrest ◽  
Gene Products ◽  
Mating Efficiency ◽  
Protein Functions ◽  
Steady State Levels ◽  
Mating Factor

The ste mutants (ste2, ste4, ste5, ste7, ste11, and ste12) are insensitive to mating factors and are, therefore, sterile. Roles of the STE gene products in the GPA1-mediated mating factor signaling pathway were studied by using ste gpa1 double mutants. Mating efficiency of a ste2 mutant defective in the alpha-factor receptor increased 1,000-fold in a gpa1 background, while G1 arrest and aberrant morphology (shmoo) caused by gpa1 were not suppressed by ste2. Furthermore, the steady-state level of the FUS1 transcript, which normally increases in response to mating factors, was also elevated when the GPA1 function was impaired. These results suggest that the GPA1 protein functions downstream of the STE2 receptor. Conversely, the sterility of ste4, ste5, ste7, ste11, and ste12 mutants was not suppressed by gpa1, but the lethal phenotype of gpa1 was suppressed by these ste mutations. Northern (RNA) blotting analysis revealed that the ste7, ste11, and ste12 mutations caused reductions of 50 to 70% in the steady-state levels of the GPA1 transcript, while ste4 had a slight effect and ste5 had no effect. This implies that the suppression by ste7, ste11, and ste12 could be due to reduced syntheses of additional components, including an effector, and that suppression by ste4 and ste5 may result from direct effects on the signaling pathway. The STE4, STE5, STE7, STE11, and STE12 products, therefore, appear to specify components of the signal transduction machinery, directly or indirectly, which function together with or downstream of GPA1.

Role of STE genes in the mating factor signaling pathway mediated by GPA1 in Saccharomyces cerevisiae

1988 ◽  
Vol 8 (9) ◽  
pp. 3777-3783
Author(s):  
N Nakayama ◽  
Y Kaziro ◽  
K Arai ◽  
K Matsumoto
Keyword(s):  
Steady State ◽  
Signaling Pathway ◽  
State Level ◽  
G1 Arrest ◽  
Gene Products ◽  
Mating Efficiency ◽  
Protein Functions ◽  
Steady State Levels ◽  
Mating Factor

The ste mutants (ste2, ste4, ste5, ste7, ste11, and ste12) are insensitive to mating factors and are, therefore, sterile. Roles of the STE gene products in the GPA1-mediated mating factor signaling pathway were studied by using ste gpa1 double mutants. Mating efficiency of a ste2 mutant defective in the alpha-factor receptor increased 1,000-fold in a gpa1 background, while G1 arrest and aberrant morphology (shmoo) caused by gpa1 were not suppressed by ste2. Furthermore, the steady-state level of the FUS1 transcript, which normally increases in response to mating factors, was also elevated when the GPA1 function was impaired. These results suggest that the GPA1 protein functions downstream of the STE2 receptor. Conversely, the sterility of ste4, ste5, ste7, ste11, and ste12 mutants was not suppressed by gpa1, but the lethal phenotype of gpa1 was suppressed by these ste mutations. Northern (RNA) blotting analysis revealed that the ste7, ste11, and ste12 mutations caused reductions of 50 to 70% in the steady-state levels of the GPA1 transcript, while ste4 had a slight effect and ste5 had no effect. This implies that the suppression by ste7, ste11, and ste12 could be due to reduced syntheses of additional components, including an effector, and that suppression by ste4 and ste5 may result from direct effects on the signaling pathway. The STE4, STE5, STE7, STE11, and STE12 products, therefore, appear to specify components of the signal transduction machinery, directly or indirectly, which function together with or downstream of GPA1.

scholarly journals Nuclear DEK preserves hematopoietic stem cells potential via NCoR1/HDAC3-Akt1/2-mTOR axis

2021 ◽  
Vol 218 (5) ◽  
Author(s):  
Zhe Chen ◽  
Dawei Huo ◽  
Lei Li ◽  
Zhilong Liu ◽  
Zhigang Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Chromatin Accessibility ◽  
Hematopoietic Stem ◽  
Chromatin Remodelers ◽  
Histone 3 ◽  
Protein Functions ◽  
Mtor Activity

The oncogene DEK is found fused with the NUP214 gene creating oncoprotein DEK-NUP214 that induces acute myeloid leukemia (AML) in patients, and secreted DEK protein functions as a hematopoietic cytokine to regulate hematopoiesis; however, the intrinsic role of nuclear DEK in hematopoietic stem cells (HSCs) remains largely unknown. Here, we show that HSCs lacking DEK display defects in long-term self-renew capacity, eventually resulting in impaired hematopoiesis. DEK deficiency reduces quiescence and accelerates mitochondrial metabolism in HSCs, in part, dependent upon activating mTOR signaling. At the molecular level, DEK recruits the corepressor NCoR1 to repress acetylation of histone 3 at lysine 27 (H3K27ac) and restricts the chromatin accessibility of HSCs, governing the expression of quiescence-associated genes (e.g., Akt1/2, Ccnb2, and p21). Inhibition of mTOR activity largely restores the maintenance and potential of Dek-cKO HSCs. These findings highlight the crucial role of nuclear DEK in preserving HSC potential, uncovering a new link between chromatin remodelers and HSC homeostasis, and have clinical implications.

Abusive head trauma (AHT) outcome at long-term follow-up and the role of elective neurosurgical approach: A report of 22 cases

2013 ◽  
Author(s):  
Francesca Menegazzo ◽  
Melissa Rosa Rizzotto ◽  
Martina Bua ◽  
Luisa Pinello ◽  
Elisabetta Tono ◽  
...  
Keyword(s):  
Head Trauma ◽  
Abusive Head Trauma ◽  
Long Term Follow Up

The Second Start of Transformation in Ukraine?

2014 ◽  
pp. 30-52 ◽  
Author(s):  
L. Grigoryev ◽  
E. Buryak ◽  
A. Golyashev
Keyword(s):  
Economic Growth ◽  
Armed Conflict ◽  
Political Crisis ◽  
Investment Climate ◽  
Institutional Reforms ◽  
Personal Consumption ◽  
Governance Quality ◽  
Political Turmoil

The Ukrainian socio-economic crisis has been developing for years and resulted in the open socio-political turmoil and armed conflict. The Ukrainian population didn’t meet objectives of the post-Soviet transformation, and people were disillusioned for years, losing trust in the state and the Future. The role of workers’ remittances in the Ukrainian economy is underestimated, since the personal consumption and stability depend strongly on them. Social inequality, oligarchic control of key national assets contributed to instability as well as regional disparity, aggravated by identity differences. Economic growth is slow due to a long-term underinvestment, and prospects of improvement are dependent on some difficult institutional reforms, macro stability, open external markets and the elites’ consensus. Recovering after socio-economic and political crisis will need not merely time, but also governance quality improvement, institutions reform, the investment climate revival - that can be attributed as the second transformation in Ukraine.

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