Related Experiment Video

Updated: Jun 27, 2026

A High-content Imaging Workflow to Study Grb2 Signaling Complexes by Expression Cloning
10:52

A High-content Imaging Workflow to Study Grb2 Signaling Complexes by Expression Cloning

Published on: October 30, 2012

Expression of the Grb2-related RET adapter protein Grap-2 in human medullary thyroid carcinoma

Leopold Ludwig1, Franz Oswald, Cuong Hoang-Vu

  • 1Department of Internal Medicine II, Klinikum rechts der Isar, University of Munich, Ismaningerstrasse 22, Munich, Germany. leopold.ludwig@lrz.tum.de

Cancer Letters
|November 26, 2008
PubMed

Insights

The adaptor Grap-2 is consistently expressed in human medullary thyroid carcinoma (MTC), suggesting a role in RET oncogenic signaling. However, genetic alterations in Grap-2 do not appear to directly influence this signaling pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • RET receptor tyrosine kinase signaling is implicated in human thyroid malignancies.
  • The adaptor protein Grap-2 has been identified as a binding partner for RET.
  • Understanding Grap-2's role is crucial for elucidating RET oncogenic signaling in thyroid cancer.

Purpose of the Study:

  • To investigate the involvement of Grap-2 in RET oncogenic signaling in human medullary thyroid carcinoma (MTC).
  • To analyze the sequence and expression of Grap-2 in MTC samples.

Main Methods:

  • Sequence analysis of the Grap-2 gene in 15 human MTC samples.
  • mRNA and protein expression analysis of Grap-2 in the same MTC samples.

Main Results:

  • All 15 MTC tumors showed significant Grap-2 mRNA and protein expression.
  • No linear correlation was observed between Grap-2 expression levels.
  • Only one conservative base pair substitution was found in the genomic Grap-2 sequence; no other significant alterations were detected.

Conclusions:

  • Consistent Grap-2 expression suggests a specific role for this adaptor in human MTC.
  • Qualitative genetic alterations in Grap-2 do not appear to be the primary drivers influencing RET signaling in MTC.

More Related Videos

Modified Yeast-Two-Hybrid System to Identify Proteins Interacting with the Growth Factor Progranulin07:56

Modified Yeast-Two-Hybrid System to Identify Proteins Interacting with the Growth Factor Progranulin

Published on: January 17, 2012

Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...