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Related Concept Videos

The Ras Gene02:38

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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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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Rab Proteins01:14

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Rab proteins constitute the largest family of monomeric GTPases, of which 70 members are present in humans. Rab proteins and their effectors regulate consecutive stages of vesicle transport such as vesicle transport, docking, and fusion to the correct recipient membrane.
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Positive feedback loop between NRASQ61R mutation and RAB27B expression in endothelial cells.

Zhi-Zheng Li1, Yu Cai2, Tian-Tian Wang1

  • 1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.

Biochemical and Biophysical Research Communications
|February 3, 2025
PubMed
Summary

The NRASQ61R mutation drives vascular anomalies by upregulating RAB27B expression in endothelial cells. Targeting RAB27B offers a potential therapeutic strategy for these conditions.

Keywords:
ERKEndotheliumNRASRAB27B

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Area of Science:

  • Endothelial cell biology
  • Molecular mechanisms of vascular anomalies
  • Small GTPase function

Background:

  • Somatic NRASQ61R mutations are implicated in vascular anomalies.
  • RAB27B regulates NRAS palmitoylation and is crucial in leukemia.
  • The role of RAB27B in NRASQ61R mutant endothelial cells remains unclear.

Purpose of the Study:

  • To investigate the role of RAB27B in NRASQ61R-mutant endothelial cells.
  • To elucidate the regulatory mechanisms of RAB27B expression in this context.
  • To identify RAB27B as a potential therapeutic target for NRAS-mutant vascular anomalies.

Main Methods:

  • Knockdown of RAB27B and RAB27A in human umbilical vein endothelial cells (HUVEC) overexpressing NRASQ61R.
  • Assessment of cell proliferation, migration, and ERK activation.
  • Analysis of RAB27B gene and protein expression levels.
  • Treatment with MEK1/2 and PI3K/mTOR inhibitors.
  • Identification of downstream transcription factors.

Main Results:

  • RAB27B knockdown inhibited proliferation and migration of NRASQ61R-HUVEC by suppressing ERK activation.
  • RAB27B expression was significantly elevated in NRASQ61R-HUVEC.
  • MEK1/2 inhibition, but not PI3K/mTOR inhibition, decreased RAB27B gene expression.
  • CCAAT enhancer binding protein beta was identified as a downstream transcription factor inducing RAB27B expression.

Conclusions:

  • A positive feedback loop exists between NRASQ61R mutation and RAB27B expression in endothelial cells.
  • RAB27B is associated with the dysfunction of NRASQ61R mutant endothelial cells.
  • RAB27B represents a promising therapeutic target for NRAS-mutant vascular anomalies.