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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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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.
Ras is a...
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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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Cytoskeletal Linker Proteins - Plakins01:09

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Plakins are large proteins with binding domains for microtubules, microfilaments, intermediate filaments, and membrane-associated protein complexes at cell junctions. Plakin functions are evolutionarily conserved and are primarily involved in organizing the different components of the cytoskeleton by crosslinking them to each other and connecting them to the cell-matrix and cell adhesion complexes. They are also known to interact with signal transducers, serve as scaffolds for signaling...
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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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Somatic to iPS Cell Reprogramming01:29

Somatic to iPS Cell Reprogramming

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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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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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Updated: Sep 11, 2025

Mouse In Vivo Placental Targeted CRISPR Manipulation
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Mouse In Vivo Placental Targeted CRISPR Manipulation

Published on: April 14, 2023

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KRAS4B is required for placental development.

Marie-Albane Minati1, Leyre López Muneta1, Younes Achouri1

  • 1Université Catholique de Louvain, de Duve Institute, Brussels, Belgium.

Cellular and Molecular Life Sciences : CMLS
|August 13, 2025
PubMed
Summary
This summary is machine-generated.

The KRAS protein is vital for embryonic development. While KRAS4B is essential for placental development and survival, KRAS4A appears to have no significant role in embryogenesis.

Keywords:
DevelopmentHeartKRAS4AKRAS4BPlacenta

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In Vitro Differentiation of Human Pluripotent Stem Cells into Trophoblastic Cells
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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Genetics

Background:

  • KRAS is essential for embryogenesis, with its absence causing embryonic lethality.
  • The specific roles of KRAS splicing isoforms, KRAS4A and KRAS4B, in development are not fully understood.

Purpose of the Study:

  • To investigate the distinct developmental roles of KRAS4A and KRAS4B.
  • To elucidate the mechanisms underlying KRAS-dependent embryonic development.

Main Methods:

  • CRISPR/Cas9 technology was used to generate Kras4A knockout (Kras4A-/-) and Kras4B knockout (Kras4B-/-) mouse models.
  • Phenotypic comparisons were made between Kras4A-/-, Kras4B-/-, and Kras-/- (double knockout) embryos.

Main Results:

  • Kras4A-/- embryos developed normally, while Kras-/- and Kras4B-/- embryos exhibited lethality around embryonic day 13.5.
  • Kras-/- embryos showed cardiac and placental defects, whereas Kras4B-/- embryos only displayed placental defects.
  • Placental defects included reduced size and glycogen trophoblast cells, leading to embryonic hypoglycemia and hypoxia.

Conclusions:

  • KRAS4B plays a predominant role in KRAS-mediated developmental functions.
  • KRAS4A may have uncharacterized functions, as Kras4A-/- mice are viable.
  • This study identifies KRAS as a key regulator of cell differentiation during development.