stuff I didnt do

Question 1

gap junctions

Answer 1

Channel forming junctions
* Main components are connexons
- consist of hexamers of connexins:
transmembrane proteins that
connect to form channels and can
open and close
* Allow passage of ions and small
2nd messenger molecules between
cells (1kD or less) and electrical signals.
* Important in epithelium, heart
muscle (signal to contract) and
neuronal synapses

Question 2

EMT

Answer 2

Epithelial-mesenchymal
transition (EMT) = change
from organised, polarised
epithelium to single
migratory cells. Proposed to
be an early step in cancer
progression
Loss of E-cadherin from cell-
cell contacts proposed to
initiate EMT as it weakens
epithelial cell contacts

Many epithelially-derived cancers have a loss
of function mutations in, or reduced
expression levels of, E-cadherin

Epithelial cells undergoes dysplasia (uncontrollable growth) form carcinoma, cells break away into blood move

Question 3

skin blistering diseases

Answer 3

Many skin blistering diseases are the result
of mutations or changes in expression of
proteins important in cell-cell adhesion
Examples include:
Pemphigus vulgaris: autoantibodies against
desmogleins 1+3 (in desmosomes). Leads
to separation of keratinocytes from each
other, and from the basal layer of the
epidermis
Epidermolysis bullosa: genetic conditions,
mutations in COLVII or Keratin genes
leading to reduced HD stability, reduced
adhesion to ECM and skin blistering

Question 4

collagens in disease

Answer 4

Fibrosis:
eg: lung, liver, skin. Characterised by excessive deposition of Collagens I or III
usually by fibroblasts. Can result in loss of tissue function - eg: in lung loss of
oxygen exchange due to decreased mechanical response
Scurvy:
Lack of Vitamin C (ascorbic acid) - essential co-factor for hydroxylases which add
hydroxyl groups to proline & lysine for stable triple-helix formation. Vitamin C
deficiency leads to formation of unstable Procollagen - vessels, tendons and skin
are fragile
Osteogenesis imperfecta (brittle bone disease):
Autosomal dominant - mutations in genes encoding 1(1) or 2(1) chains (Type
I collagen). Glycine mutated (critical to triple helix formation) resulting in helices
that are poorly formed and unstable.

Question 5

fibroblasts and cancer

Answer 5

Fibroblast Movement and Cancer Metastasis
Fibroblasts play an important role in moving through the collagen matrix by generating mechanical forces that interact dynamically with the ECM. In cancer, the fibronectin matrix and the behavior of fibroblasts change to facilitate metastasis. Fibroblasts undergo a phenotypic switch to an ameboid phenotype, enabling them to invade tissues and spread throughout the body, contributing to cancer progression. The forces exerted by fibroblasts on the ECM are critical in processes such as tissue remodeling, wound healing, and cancer metastasis.