Mouse lymphoma cells with mutations of cyclic AMP-dependent protein kinase

National Cancer Institute Monograph
|May 1, 1978
PubMed

Insights

Researchers studied cyclic AMP (cAMP) signaling in S49 cells. Mutants with defects in cAMP-dependent protein kinase were identified and characterized, providing insights into cellular responses.

Area of Science:

  • Cellular biology
  • Molecular genetics
  • Signal transduction

Background:

  • S49 cells are sensitive to cyclic AMP (cAMP) mediated cell death.
  • Mutants with altered cAMP signaling can be selected based on this sensitivity.
  • Defects in cAMP-dependent protein kinase represent one class of such mutants.

Purpose of the Study:

  • To select and characterize mutants with defects in cAMP signaling pathways.
  • To investigate the role of cAMP-dependent protein kinase in cellular responses.
  • To understand the genetic and biochemical basis of cAMP signaling.

Main Methods:

  • Selection of S49 cell mutants resistant to cAMP-induced killing.
  • Genetic characterization of selected mutants.
  • Biochemical analysis of cAMP-dependent protein kinase function.

Main Results:

  • Identification of multiple classes of mutants affecting cAMP generation or response.
  • Extensive genetic and biochemical characterization of mutants deficient in cAMP-dependent protein kinase.
  • Detailed analysis of the cAMP-dependent protein kinase pathway.

Conclusions:

  • S49 cell mutants provide a powerful tool for dissecting cAMP signaling.
  • Mutations in cAMP-dependent protein kinase significantly impact cellular cAMP responses.
  • Comprehensive characterization of these mutants deepens understanding of cAMP-mediated cellular processes.

Related Concept Videos

Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...