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TLS Online TPP Program

#Question id: 5059

The responding tissue has already been specified and needs only an environment that allows the expression of these traits, process called as

#SCPH01 Biochemistry

  1. Epithelial-mesenchymal interactions

  2. Reciprocal inductions

  3. Instructive interactions

  4. Permissive interactions

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TLS Online TPP Program

#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.
TLS Online TPP Program

#Question id: 7764

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

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.
TLS Online TPP Program

#Question id: 7764

#SCPH06 I Botany

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.
TLS Online TPP Program

#Question id: 7764

#SCPH28 | Zoology

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.