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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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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
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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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.
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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: Dec 30, 2025

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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SOCS1: phosphorylation, dimerization and tumor suppression.

Frédéric Lessard1, Emmanuelle Saint-Germain1, Lian Mignacca1

  • 1Département de Biochimie et Médecine Moléculaire, Université de Montréal, Montréal, Québec, Canada.

Oncoscience
|January 28, 2020
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Summary
This summary is machine-generated.

Suppressor of cytokine signaling (SOCS) proteins inhibit JAK-STAT signaling and tumor suppression. Reactivating the SOCS1-p53 axis with dasatinib and PRIMA offers new cancer treatment strategies.

Keywords:
P53SH2 domainsSRC kinasescytokine singling

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Suppressor of cytokine signaling (SOCS) proteins regulate cell growth, differentiation, and apoptosis.
  • SOCS1 and SOCS3 are implicated in tumor suppression via interaction with p53.
  • SRC family kinases (SFK) phosphorylate SOCS1, inhibiting its tumor suppressor function.

Purpose of the Study:

  • To investigate the role of SFK in SOCS1 regulation.
  • To explore therapeutic strategies for reactivating the SOCS1-p53 tumor suppressor axis.

Main Methods:

  • Investigated SOCS1 phosphorylation by SFK.
  • Utilized SFK inhibitor dasatinib and p53 activator PRIMA.
  • Assessed reactivation of the SOCS1-p53 axis.

Main Results:

  • SRC family kinases phosphorylate SOCS1, inhibiting its interaction with p53.
  • Dasatinib in combination with PRIMA reactivated the SOCS1-p53 tumor suppressor axis.

Conclusions:

  • SFK activity disrupts SOCS1-mediated tumor suppression.
  • Targeting SFK and p53 presents a novel therapeutic approach for cancer treatment.