answer

watching

views

11 Oct 2018

Outline the role that the Ubiquitin degradation pathway plays in Wnt signaling. Give two examples of DNA mutations that could affect targeting to this pathway and lead to the over proliferation of cells (i.e. the Wnt pathway always being turned on).

answer

watching

views

For unlimited access to Homework Help, a Homework+ subscription is required.

You have 0 free answers left.
Get unlimited access to 3.8 million step-by-step answers.

Get unlimited access

Already have an account? Log in

Sixta KovacekLv2

13 Oct 2018

Unlock all answers

Get 1 free homework help answer.

Already have an account? Log in

Related questions

Her2 is an EGF receptor family member that drives proliferation of cells including in the breast. Too much Her2 signaling can contribute to Her2 positive breast cancer. Mutations can be generated in different proteins in the Her2 signaling pathway. The following are 5 different possible mutations.

Mutant a: Ras protein that cannot exchange GDP for GTP.

Mutant b: RAF protein with a mutation in the active site such that ATP does not bind.

Mutant c: Her2 receptor that lacks tyrosines in its intracellular domain.

Mutant d: MAPK that is constitutively active.

Mutant e: Myc expressed 10X higher than normal.

The following cell lines with mutations in Her2, Ras/MAPK pathway are treated with the ligand for the Her2 receptor and compared to normal cells treated with ligand. For each Her2 mutant pathway cell line, describe whether myc synthesis is higher or lower compared to normal cells and if proliferation (cell division) is higher or lower compared to normal cells treated with ligand

A. Cell line with mutations a and b.

B. Cell line with mutations c and e

C. Cell line with mutations d and e

D. Rb is also important for regulation of the cell cycle at the restriction point or start. What would be the effect on myc and cell proliferation of a mutation that switched all the serines and threonines that are phosphorylated to alanine?

please solve this:

Cancer Biology (Oncogenic Pathways)

The majority of malignant cells rely on dysregulation of a handful of oncogenes and their associated signaling pathways to support their abnormal proliferation and survival. The list below indicates the proteins that have become the âname sakeâ for these key dysregulated pathways. Note that sometimes the protein listed is mutated and drives the pathway (ex. Ras), but other times it is rarely mutated (ex. Akt where PI3K and PTEN mutations predominate).

Working together in your groups, please create a portfolio of âprofilesâ for the pathways shown below. For each pathway, include a map that links together the main proteins or molecules involved- ligands, receptors, transcription factors, etc... but always end with the ultimate effect on the cell! These pathway maps must be your own creation- do not copy other image files. For each protein or molecule you list in the map, please provide a âkeyâ that describes what it is, its specific function in the pathway, and detail where the most common pathogenic mutations occur in at least three proteins in the pathway (see below for details). Since these pathways can be extremely complex, you need not include more than three proteins or molecules at any one level in the pathway.

For information on the pathogenic mutations, use the COSMIC (catalogue of somatic muations in cancer) resource at http://cancer.sanger.ac.uk/cosmic . Enter the gene/protein name Ã click on the gene name in table below Ã under âMutation Impactâ select Pathogenic Ã Apply. A bar graph depicting the various mutations will be shown, provide the number of confirmed mutations and the changes (DNA and amino acids) it causes at that site. For example, in the BRAF gene: 24,291 mutations have been confirmed that involve a T to A mutation at base 1799 which leads to a Valine (V) to Glutamic acid (E) amino acid substitution at position 600 (note this mutation constitutively activates the BRaf kinase).

Key Oncogenic Pathways to Profile:

Ras

Akt

Wnt

TGFB

Notch

Hedgehog

Grading will be based on aesthetic clarity, thoroughness and accuracy of the information.

Grading Rubric: 75 points total

Visuals: Aesthetic clarity 30 points

Pathways are well organized, easy to follow

activating and inhibitory relationships are readily apparent

Creative layout

Content: Thoroughness and Accuracy 30 points

All pathways completed

Essential level of detail in key

The lab you work in has discovered a previously unidentified extracellular signal molecule called QGF. You add purified QGF to different types of cells to determine its effect on these cells. When you add QGF to heart muscle cells, you observe an increase in cell contraction. When you add it to fibroblasts, they undergo cell division. When you add it to nerve cells, they die. When you add it to glial cells, you do not see any effect on cell division or survival.

A) How can the same signaling molecule cause such diverse affects? Why do the glial cells not respond at all?

B) Using effectors and second messengers discussed in class, devise a signaling pathway that QGF could use to increase contractions in in the heart. (Hint: Ca2+ is very important for muscle contraction)

C) Using effectors and second messengers discussed in class, devise a signaling pathway that QGF could use to lead to apoptosis of nerve cells. Give possible proteins or genes that need to be activated or inactivated.

D) Using effectors and second messengers discussed in class, devise a signaling pathway that QGF could use to induce cell division in the fibroblast cells? Give possible proteins or genes that need to be activated or inactivated.