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TLS Online TPP Program

#Question id: 1278

Vertebrate gap junctions are composed of:

#Unit 4. Cell Communication and Cell Signaling

  1. adherins.

  2. collagens.

  3. connexins.

  4. integrins

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TLS Online TPP Program

#Question id: 7316

#Unit 5. Developmental Biology

Programmed cell death, or apoptosis, is an essential part of animal development. In the nematode, with its invariant cell lineage, particular cell lineages or particular cells within specific lineages are destined to end in programmed cell death, and it was this feature that allowed the identification of the process and the analysis of its genetic control.

Which of the following combination of genes are correct?
TLS Online TPP Program

#Question id: 7754

#Unit 5. Developmental Biology

In autophagy, the endoplasmic reticulum (ER) first gives rise to a cup-shaped, membranous cisterna called the
TLS Online TPP Program

#Question id: 7755

#Unit 5. Developmental Biology

which type of complex is required for movement of ATG9 from the phagophore assembly site to the peripheral site, where it obtains fresh membrane?
TLS Online TPP Program

#Question id: 7757

#Unit 5. Developmental Biology

The TOR (target of rapamycin) kinase complex acts as a
TLS Online TPP Program

#Question id: 7761

#Unit 5. Developmental Biology

Correct sets of genes are well known to be involved in aging and its prevention, and each set appears to be conserved between phyla and even kingdoms. 
a. DNA repair enzymes
b. proteins of the insulin signaling pathway
c. proteins in the mTORC1 signaling pathway
d. chromatin remodeling enzymes
TLS Online TPP Program

#Question id: 7764

#Unit 5. Developmental Biology

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.