TLS Online TPP Program

#Question id: 6956


The central nervous system is derived from _____, the axial skeleton is derived from _____, and the muscles of the trunk are derived from _____?

#SCPH01 Biochemistry
  1. ectoderm, mesoderm, endoderm
  2. mesoderm, endoderm, endoderm
  3. ectoderm, mesoderm, mesoderm
  4. all are derived from mesoderm
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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.

TLS Online TPP Program

#Question id: 7765

#SCPH01 Biochemistry

The enzyme complex or gene that maintains telomere integrity is________, which acts as an antisenescence complex. Mice and humans with its deficiencies age prematurely (Mitchell et al. 1999). Overexpressing or reactivating it in senescent cells extends longevity in mice without increasing cancer,

TLS Online TPP Program

#Question id: 7765

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

The enzyme complex or gene that maintains telomere integrity is________, which acts as an antisenescence complex. Mice and humans with its deficiencies age prematurely (Mitchell et al. 1999). Overexpressing or reactivating it in senescent cells extends longevity in mice without increasing cancer,