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Related Concept Videos

M-Cdk Drives Transition Into Mitosis02:15

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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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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.
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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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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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Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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Updated: Sep 19, 2025

Identification of Novel CK2 Kinase Substrates Using a Versatile Biochemical Approach
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CDKL3, a versatile kinase with increasing recognition.

Lanjing Ma1, Haijiao Zhang1, Zhongqiu Pang1

  • 1College of Life and Health Sciences, Northeastern University, Shenyang, 110819, China.

Biochemical and Biophysical Research Communications
|June 4, 2025
PubMed
Summary
This summary is machine-generated.

Cyclin-Dependent Kinase-Like 3 (CDKL3) plays a key role in cell cycle regulation and metabolic diseases. Recent studies reveal its pivotal functions in cancer initiation and progression, warranting further investigation.

Keywords:
AktCDKL3Cell cycleMetabolismOncogeneccRCC

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Area of Science:

  • Molecular Biology
  • Biochemistry
  • Oncology

Background:

  • Cyclin-Dependent Kinase-Like 3 (CDKL3) is a serine/threonine kinase in the CDKL family, identified in 1999.
  • Despite structural similarities to MAPK and CDK, CDKL3's functions have been historically under-explored.
  • Previous research indicated CDKL3 involvement in cell cycle regulation and cancer, but mechanisms remain unclear.

Purpose of the Study:

  • To comprehensively review the molecular mechanisms, functions, and protein interactions of CDKL3.
  • To elucidate the pivotal role of CDKL3 in cell cycle regulation, metabolic disease, and cancer.
  • To discuss future research perspectives for CDKL3.

Main Methods:

  • Systematic review of existing literature on CDKL3.
  • Analysis of CDKL3's molecular structure and sequence homology.
  • Integration of recent findings on CDKL3's physiological roles.

Main Results:

  • CDKL3 is confirmed to be pivotal in cell cycle regulation.
  • CDKL3 significantly impacts metabolic disease development.
  • CDKL3 plays a crucial role in cancer initiation and progression.

Conclusions:

  • CDKL3 is a key regulator with significant implications in cell cycle control and metabolic health.
  • Further research into CDKL3's mechanisms is essential for understanding and potentially treating cancer.
  • CDKL3 represents a promising target for future therapeutic strategies.