Related Experiment Video

Updated: Mar 19, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

9.2K

HIPK2 modification code for cell death and survival

Dong Wook Choi1, Cheol Yong Choi1

  • 1Department of Biological Sciences; Sungkyunkwan University ; Suwon, Republic of Korea.

Molecular & Cellular Oncology
|June 17, 2016
PubMed

Insights

Homeodomain-interacting protein kinase 2 (HIPK2) acts as a crucial signal transducer. Its unique "HIPK2 modification code" of post-translational modifications dictates cellular responses to DNA damage and maintains cell fate.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Homeodomain-interacting protein kinase 2 (HIPK2) is a serine/threonine kinase involved in regulating cellular activities.
  • It functions as a transcriptional cofactor and signal transducer, impacting development, cell cycle, proliferation, differentiation, and DNA damage response.

Purpose of the Study:

  • To elucidate the regulatory mechanisms of HIPK2.
  • To investigate the role of post-translational modifications in HIPK2 function and cellular signaling.

Main Methods:

  • Analysis of HIPK2 post-translational modifications, including polyubiquitination, SUMOylation, phosphorylation, and acetylation.
  • Investigating how these modifications integrate signaling cues and cellular stimuli.

Main Results:

  • HIPK2 function is modulated by its catalytic activity, stability, and localization, all influenced by post-translational modifications.
  • HIPK2 undergoes combinatorial modifications, termed the "HIPK2 modification code," rather than individual modifications.
  • Unique modification patterns of HIPK2 reflect its integration of signaling cues and response to DNA damage and ROS levels.

Conclusions:

  • The "HIPK2 modification code" is essential for integrating diverse cellular signals and determining cell fate.
  • HIPK2 modification patterns are context-dependent, influencing cellular homeostasis and cell fate decisions.
Keywords:
DNA damage responseDNA repairHIPK2SUMOylationapoptosiscaspase cleavagephosphorylationubiquitination

More Related Videos

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells12:44

Use of LysoTracker to Detect Programmed Cell Death in Embryos and Differentiating Embryonic Stem Cells

Published on: October 11, 2012

24.1K
Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter11:32

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

7.5K

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
10.9K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
6.1K
Abnormal Proliferation02:23

Abnormal Proliferation

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...
5.4K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.2K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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...
6.2K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
9.1K