scholarly journals Stimulation of the cell cycle and maize transformation by disruption of the plant retinoblastoma pathway

2002 ◽  
Vol 99 (18) ◽  
pp. 11975-11980 ◽  
Author(s):  
W. Gordon-Kamm ◽  
B. P. Dilkes ◽  
K. Lowe ◽  
G. Hoerster ◽  
X. Sun ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Maize Transformation ◽  
Stimulation Of

scholarly journals Integrin-mediated Activation of Focal Adhesion Kinase Is Required for Signaling to Jun NH2-terminal Kinase and Progression through the G1 Phase of the Cell Cycle

1999 ◽  
Vol 145 (7) ◽  
pp. 1461-1470 ◽  
Author(s):  
Maja Oktay ◽  
Kishore K. Wary ◽  
Michael Dans ◽  
Raymond B. Birge ◽  
Filippo G. Giancotti
Keyword(s):  
Cell Cycle ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
G1 Phase ◽  
Normal Cells ◽  
Jnk Signaling ◽  
Stringent Control ◽  
No Activation ◽  
Stimulation Of

The extracellular matrix exerts a stringent control on the proliferation of normal cells, suggesting the existence of a mitogenic signaling pathway activated by integrins, but not significantly by growth factor receptors. Herein, we provide evidence that integrins cause a significant and protracted activation of Jun NH2-terminal kinase (JNK), while several growth factors cause more modest or no activation of this enzyme. Integrin-mediated stimulation of JNK required the association of focal adhesion kinase (FAK) with a Src kinase and p130CAS, the phosphorylation of p130CAS, and subsequently, the recruitment of Crk. Ras and PI-3K were not required. FAK–JNK signaling was necessary for proper progression through the G1 phase of the cell cycle. These findings establish a role for FAK in both the activation of JNK and the control of the cell cycle, and identify a physiological stimulus for JNK signaling that is consistent with the role of Jun in both proliferation and transformation.

scholarly journals Changes in numbers of prolactin receptors during the cell cycle of Nb2 cells

1998 ◽  
Vol 159 (1) ◽  
pp. R1-R4
Author(s):  
IG Camarillo ◽  
JA Rillema
Keyword(s):  
Cell Cycle ◽  
Specific Binding ◽  
Prolactin Receptors ◽  
Initial Value ◽  
Cellular Processes ◽  
Nb2 Cells ◽  
Signalling Molecule ◽  
Lactogenic Hormones ◽  
T Lymphoma ◽  
Stimulation Of

Lactogenic hormones including prolactin (PRL) have mitogenic effects on Nb2 cells, a pre-T lymphoma cell line. Previous studies have characterized the PRL stimulation of cellular processes such as RNA/DNA synthesis, signalling molecule activation, and the expression of specific genes. The data presented here explores the fluctuations in plasma membrane PRL receptor (PRLR) number that occur in the Nb2 cells during the course of a 24 h cell cycle. PRLR abundance was determined by measuring specific binding of [I125] oPRL to G1 arrested-intact Nb2 cells in which the cell cycle was initiated by addition of nonradioactive oPRL. Preliminary studies revealed that 1 ng/ml oPRL was the minimum PRL concentration that causes a maximal stimulation of mitogenesis, without interfering with [I125] oPRL binding measurements. Subsequent experiments revealed that upon cell cycle initiation of G1 arrested Nb2 cells with 1 ng/ml oPRL, PRLR number remained constant for the initial 6 h. After 8 h PRLR numbers decreased and at 12 h, the PRLR number was less than 25% of the initial value. After 12 hr, PRLR numbers increased and reach initial values by 18 hr. These studies show that the expression of cell surface PRL receptors is modulated in a sequential fashion during the cell cycle of Nb2 cells.

Microinjection of fos-specific antibodies blocks DNA synthesis in fibroblast cells

1988 ◽  
Vol 8 (4) ◽  
pp. 1670-1676 ◽  
Author(s):  
K T Riabowol ◽  
R J Vosatka ◽  
E B Ziff ◽  
N J Lamb ◽  
J R Feramisco
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Antisense Rna ◽  
Proliferating Cells ◽  
Rna Transcripts ◽  
Serum Stimulation ◽  
Inhibition Of Growth ◽  
Nonspecific Immunoglobulins ◽  
3T3 Cell Lines ◽  
Stimulation Of

Transcription of the protooncogene c-fos is increased greater than 10-fold within minutes of treatment of fibroblasts with serum or purified growth factors. Recent experiments with mouse 3T3 cell lines containing inducible fos antisense RNA constructs have shown that induced fos antisense RNA transcripts cause either a marked inhibition of growth in continuously proliferating cells or, conversely, a minimal effect except during the transition from a quiescent (G0) state into the cell cycle. Since intracellular production of large amounts of antisense RNA does not completely block gene expression, we microinjected affinity-purified antibodies raised against fos to determine whether and when during the cell cycle c-fos expression was required for cell proliferation. Using this independent method, we found that microinjected fos antibodies efficiently blocked serum-stimulated DNA synthesis when injected up to 6 to 8 h after serum stimulation of quiescent REF-52 fibroblasts. Furthermore, when fos antibodies were injected into asynchronously growing cells, a consistently greater number of cells was prevented from synthesizing DNA than when cells were injected with nonspecific immunoglobulins. Thus, whereas the activity of c-fos may be necessary for transition of fibroblasts from G0 to G1 of the cell cycle, its function is also required during the early G1 portion of the cell cycle to allow subsequent DNA synthesis.

Induction of yeast histone genes by stimulation of stationary-phase cells

1990 ◽  
Vol 10 (12) ◽  
pp. 6356-6361
Author(s):  
M A Drebot ◽  
L M Veinot-Drebot ◽  
R A Singer ◽  
G C Johnston
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Stationary Phase ◽  
Mitotic Cell ◽  
Specific Gene ◽  
Mitotic Cell Cycle ◽  
Histone Genes ◽  
Yeast Saccharomyces Cerevisiae ◽  
Alpha Factor ◽  
Stimulation Of

In the cell cycle of the budding yeast Saccharomyces cerevisiae, expression of the histone genes H2A and H2B of the TRT1 and TRT2 loci is regulated by the performance of "start," the step that also regulates the cell cycle. Here we show that histone production is also subject to an additional form of regulation that is unrelated to the mitotic cell cycle. Expression of histone genes, as assessed by Northern (RNA) analysis, was shown to increase promptly after the stimulation, brought about by fresh medium, that activates stationary-phase cells to reenter the mitotic cell cycle. The use of a yeast mutant that is conditionally blocked in the resumption of proliferation at a step that is not part of the mitotic cell cycle (M.A. Drebot, G.C. Johnston, and R.A. Singer, Proc. Natl. Acad. Sci. 84:7948, 1987) showed that this increased gene expression that occurs upon stimulation of stationary-phase cells took place in the absence of DNA synthesis and without the performance of start. This stimulation-specific gene expression was blocked by the mating pheromone alpha-factor, indicating that alpha-factor directly inhibits expression of these histone genes, independently of start.

scholarly journals Stimulierung von Kulturen embryonaler Rattenzellen durch eine Proteinfraktion aus fötalem Kälberserum / Stimulation of Embryonic Rat Cells in Culture by a Protein Fraction Isolated from Fetal Calf Serum

1971 ◽  
Vol 26 (10) ◽  
pp. 1045-1048 ◽  
Author(s):  
Dieter F. Hülser ◽  
Werner Frank
Keyword(s):  
Cell Cycle ◽  
Culture Medium ◽  
Fetal Calf Serum ◽  
Surface Membrane ◽  
Calf Serum ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Membrane Potential Difference ◽  
Stimulation Of

Normal embryonic rat cells incubated in serum-free medium accumulate in G1-phase of the cell cycle. On addition of a growth-stimulating protein isolated from fetal calf serum they are triggered to proceed through the cycle, and they resume DNA-synthesis 15 to 20 hours later. In this paper it is demonstrated that the surface membrane potential difference (PD) decreases immediately after changing serum-free medium against culture medium containing either calf serum or the isolated serum protein; the original PD is restored 2 to 3 hours later. Serumprotein without growthstimulating activity does not affect the PD.A permanent rat cell line which grows independently of serum also has been tested. The PD of these cells is not significantly influenced by calf serum.

Stimulation of Human Breast Cancer MCF-7 Cells with Estrogen Prevents Cell Cycle Arrest by HMG-CoA Reductase Inhibitors

1996 ◽  
Vol 220 (3) ◽  
pp. 864-870 ◽  
Author(s):  
R. Addeo ◽  
L. Altucci ◽  
T. Battista ◽  
I.M. Bonapace ◽  
M. Cancemi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Reductase Inhibitors ◽  
Cycle Arrest ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase ◽  
Mcf 7 ◽  
Stimulation Of

scholarly journals Stat Proteins Control Lymphocyte Proliferation by Regulating p27Kip1 Expression

1998 ◽  
Vol 18 (4) ◽  
pp. 1996-2003 ◽  
Author(s):  
Mark H. Kaplan ◽  
Carla Daniel ◽  
Ulrike Schindler ◽  
Michael J. Grusby
Keyword(s):  
Cell Cycle ◽  
Proliferative Response ◽  
S Phase ◽  
Interleukin 4 ◽  
Activated T Cells ◽  
Stat Proteins ◽  
Protein Levels ◽  
Proliferation Of Lymphocytes ◽  
Cytokine Stimulation ◽  
Stimulation Of

ABSTRACT The proliferation of lymphocytes in response to cytokine stimulation is essential for a variety of immune responses. Recent studies with signal transducer and activator of transcription 6 (Stat6)-deficient mice have demonstrated that this protein is required for the normal proliferation of lymphocytes in response to interleukin-4 (IL-4). In this report, we show that the impaired IL-4-induced proliferative response of Stat6-deficient lymphocytes is not due to an inability to activate alternate signaling pathways, such as those involving insulin receptor substrates, or to a failure to upregulate IL-4 receptor levels. Cell cycle analysis showed that the percentage of Stat6-deficient lymphocytes that transit from the G1 to the S phase of the cell cycle following IL-4 stimulation is lower than that of control lymphocytes. Although the regulation of many genes involved in the control of cytokine-induced proliferation is normal in Stat6-deficient lymphocytes, protein levels of the cdk inhibitor p27Kip1 were found to be markedly dysregulated. p27Kip1 is expressed at significantly higher levels in Stat6-deficient lymphocytes than in control cells following IL-4 stimulation. The higher level of p27Kip1 expression seen in IL-4-stimulated Stat6-deficient lymphocytes correlates with decreased cdk2-associated kinase activity and is the result of the increased accumulation of protein rather than altered mRNA expression. Similarly, higher levels of p27Kip1 protein expression are also seen following IL-12 stimulation of Stat4-deficient lymphocytes than are seen following stimulation of control cells. These data suggest that Stat proteins may control the cytokine-induced proliferative response of activated T cells by regulating the expression of cell cycle inhibitors so that cyclin-cdk complexes may function to promote transition from the G1 to the S phase of the cell cycle.

Stimulation of DNA synthesis by adenosine diphosphoribosylation of HeLa nuclear proteins during the cell cycle

1973 ◽  
Vol 52 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Jerry H. Roberts ◽  
Patricia Stark ◽  
Mark Smulson
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Nuclear Proteins ◽  
Stimulation Of

Alteration of Cell Cycle Kinetics and Immunoglobulin Gene Transcription as the Result of Multiple Agonist Stimulation of Murine B Cells

1994 ◽  
Vol 155 (1) ◽  
pp. 156-168 ◽  
Author(s):  
Teri L. Jones ◽  
Louise Barnett ◽  
David Lafrenz
Keyword(s):  
Cell Cycle ◽  
B Cells ◽  
Gene Transcription ◽  
Immunoglobulin Gene ◽  
Cell Cycle Kinetics ◽  
Agonist Stimulation ◽  
Stimulation Of
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