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Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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MAPK Signaling Cascades01:07

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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...
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mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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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...
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Non-Canonical Wnt Signaling Pathways01:41

Non-Canonical Wnt Signaling Pathways

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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Updated: Oct 20, 2025

A Robust Discovery Platform for the Identification of Novel Mediators of Melanoma Metastasis
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Canonical Signaling Pathways in Melanoma.

Lillian Sun1, Joshua Arbesman2

  • 1Cleveland Clinic, Lerner College of Medicine at Case Western Reserve University, 9501 Euclid Avenue, Cleveland, OH 44106, USA.

Clinics in Plastic Surgery
|September 10, 2021
PubMed
Summary
This summary is machine-generated.

This review details key genetic mutations and signaling pathways driving melanoma, the deadliest skin cancer. Understanding these mechanisms is crucial for developing effective melanoma treatments.

Keywords:
Drug targetsMelanomaMutationsSignaling pathwaysTumorigenesis

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Area of Science:

  • Oncology
  • Dermatology
  • Molecular Biology

Background:

  • Melanoma is the most lethal form of skin cancer.
  • It arises from uncontrolled melanocyte proliferation.
  • Understanding melanoma pathogenesis is key for new therapies.

Purpose of the Study:

  • To review key signaling pathways in melanoma.
  • To identify driver mutations in melanoma tumorigenesis.
  • To discuss potential underlying mechanisms of melanoma development.

Main Methods:

  • Literature review of melanoma research.
  • Analysis of genetic mutations and signaling pathways.
  • Synthesis of current understanding of melanoma pathogenesis.

Main Results:

  • Identification of critical signaling pathways implicated in melanoma.
  • Pinpointing of specific driver mutations contributing to melanoma.
  • Elucidation of molecular mechanisms driving melanoma progression.

Conclusions:

  • Driver mutations and signaling pathways are central to melanoma.
  • Further research into these mechanisms can guide therapeutic strategies.
  • A comprehensive understanding is vital for combating melanoma.