Cell cycle is regulated by master regulators (cyclin and CDKs). In vertebrates, G1 CDK activity rises during G1 and is stimulated by the presence of growth factors. When signaling from growth factors is sustained, the resulting cyclin D–CDK4/6 complexes begin phosphorylating Rb, releasing some E2F, which stimulates transcription of the genes encoding cyclin E, CDK2, and E2F itself. In a particular cell type there is a mutation in Rb such that it cannot be phosphorylated. What will be the correct expression pattern of cyclin E in these cells after mitotic stimulation?

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#Question id: 7762

#SCPH28 | Zoology

Correlation between life span and the ability of fibroblasts to repair DNA in various mammalian species, Repair capacity is represented in autoradiography by the number of grains from radioactive thymidine per cell nucleus. According to graph, which factor exist on x-axis ? Note that the y-axis (life span) is logarithmic.

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#Question id: 7763

#SCPH01 Biochemistry

Two major sources of mutation are radiation and reactive oxygen species (ROS).The reactive oxygen species hypothesis for aging postulates that 

1) Senescence results from the accumulation of DNA, lipid, and protein damage inflicted by ROS of mitochondrial origin; and

2) Mitochondria of long-lived species should produce high ROS than do mitochondria of short-lived species.

3) the capacity of mitochondria to consume ROS might distinguish long-lived species from short-lived species, rather than differences in ROS generation. 

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#Question id: 7763

#I Life Science/ Life Sciences Group – I-V

Two major sources of mutation are radiation and reactive oxygen species (ROS).The reactive oxygen species hypothesis for aging postulates that 

1) Senescence results from the accumulation of DNA, lipid, and protein damage inflicted by ROS of mitochondrial origin; and

2) Mitochondria of long-lived species should produce high ROS than do mitochondria of short-lived species.

3) the capacity of mitochondria to consume ROS might distinguish long-lived species from short-lived species, rather than differences in ROS generation. 

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#Question id: 7763

#SCPH06 I Botany

Two major sources of mutation are radiation and reactive oxygen species (ROS).The reactive oxygen species hypothesis for aging postulates that 

1) Senescence results from the accumulation of DNA, lipid, and protein damage inflicted by ROS of mitochondrial origin; and

2) Mitochondria of long-lived species should produce high ROS than do mitochondria of short-lived species.

3) the capacity of mitochondria to consume ROS might distinguish long-lived species from short-lived species, rather than differences in ROS generation. 

TLS Online TPP Program

#Question id: 7763

#SCPH28 | Zoology

Two major sources of mutation are radiation and reactive oxygen species (ROS).The reactive oxygen species hypothesis for aging postulates that 

1) Senescence results from the accumulation of DNA, lipid, and protein damage inflicted by ROS of mitochondrial origin; and

2) Mitochondria of long-lived species should produce high ROS than do mitochondria of short-lived species.

3) the capacity of mitochondria to consume ROS might distinguish long-lived species from short-lived species, rather than differences in ROS generation. 

TLS Online TPP Program

#Question id: 7764

#SCPH01 Biochemistry

Cellular senescence may have evolved to protect organisms against cancer. Instead of dividing out of control, the cells die. Cellular senescence appears to be regulated by several tumor suppressor genes, especially p53.what is the most appropriate reason behind this,

1) Transcription factor p53 is thought to suppress tumorigenesis by causing cell arrest and senescence in response to short telomeres, DNA damage, and viral or external signals to divide

2) This factor can stop the cell cycle, cause cellular senescence in rapidly dividing cells, instruct genes to initiate cellular apoptosis, and activate DNA repair enzymes.

3) Induction of apoptosis or cellular senescence by p53 always beneficial.