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70 Cards in this Set
- Front
- Back
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signal transductiion of GF |
through membrane receptors to: 1. ion channels (according to gradient) 2. G proteins (activ. of mem. enzymes) 3. receptor kinases (direct. activ. signalling cascase) |
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ion channels |
free flow of small inos according to concentration gradient can open and close according to stimuli |
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G protein signalling |
alpha+beta+gamma subunits mediate cell response to extracellular stimuli |
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extracellular transcription signals |
1. TGF\BMP 2. notch 3. FGF 4. Wnt 5. hedghod |
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no. of genes encoding to PTK (protein tyrosin kinase) |
58 genes |
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strictire pf tyrosin kinase |
1. extracellualr domain 2. intracellualr domain 3. transmembrane domain |
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action of tyrosin kinase receptor |
1. ligand activated 2. dimerization 3. intracellualr domain get closer 4. autophosphorolation 5. triggers downstream signalling cascase 6. activation of multiple signal molecules |
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canonical signalling pathway |
1. FGF attached to FGF receptor 2. activated 3. initiates Ras\Raf pathway |
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genetic abnormalities in the FGFr |
1. cancer 2. chromosmal transclocation 3. gene amplification\ overexpression 4. mutation activation |
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FGF10 ligand codes for |
limb bud growth |
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Vegfa codes for? |
angiogenesis |
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FGF10 |
GF of mesenchymal proliferation, builds limb bud |
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FGFR3 |
receptor of FGF malfunction- giant individual |
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indian hedghod |
morphogen shutting fown will lead giaganitism |
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criteria of stem cells |
1. self renewal 2. differentiation |
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what kind of division does the embryonic stem cells go through? |
symmetrical division |
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what kind of division does the feotal and adult stem cells go through? |
asymmetrical divisio |
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type of totipotency |
zygot |
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type of pluripotency |
embryonic SC |
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type of multipotency |
hematopoeitic SC |
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type of oligopotency |
gastrointestinal SC |
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type of unipotency |
prostate SC |
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niche |
presence of several types of supportive cells and signalling molecules |
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induced pluripotency |
by transcription factors oct4 sox2 c-Myc klf4 |
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where can embryonic stem cell proliferate? |
in vitro in vivo |
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characteristic of adult stem cells |
residue in several organs have self renewal capitability can generate differentiation |
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commitment of stem cells |
the differentiation is restricted to a specific cell in the future |
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autonomous scecifity of stem cells |
no need for external signal to differentiate (embryonic stem cell) |
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conditional specification |
in adult cells gets external signals from neighbohrong cells to how to differentiate |
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organoids |
organ bud grown in vitro |
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aneuploidy |
an abnormal number of chromsomes in cell (45\47) |
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euploidy |
having a complete extra set of chromsomes |
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transition mutation |
switching of purin with another purin (or pyrimidin with another pyrimidin) |
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tranverstion mutation |
switching of purin with pyrimidin and vice versa |
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exogenous DNA alternation sources |
UV pollution smoking food ionizing radiation xray chemotherapy |
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endogenous DNA alternation sources |
replication errors spontaneous DNA alternation alkylating agents |
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what kind of damage does UV cause? |
covalent bond btw neighborhing Thymin (thymin dimers) |
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deamination |
base exchange |
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depurination |
deletation |
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intercalating mutagenes |
are "like base" and fit btw adjacent base pairs lead to transitional frameshifts |
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how many mutation occurs per day in a cell |
500,000 |
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how many cell division occurs during life |
10^16 |
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base excision repare |
1. DNA glycosylase recognizes a wrong base 2. DNA glycosylase removes the wrong base 3. AP nuclase stays on the gap created 4. DNA pol. fills the gap with the correct base 5. DNA ligase connects the adj. parts of the same strand |
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nucleotise excision repaire |
dimers occuring btw same strand 1. uvrA+uvrB recognize mistake 2. uvrB remaines attached to mistake 3.uvrC attaches to the area 4. uvrC cuts one strand away from mistake 5. hilcase separates the 2 strands 6. DNA pol. III fills the gap 7. DNA ligase connects the same strand |
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mismatch repair |
when wrong base are paired (during replication) 1. Muts recongnizes mismatch 2. MutH creates a "nick" in the new strand 3. exonuclease removes the new and marked strand 4. DNA pol. builds new strand 5. ligase |
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falconi anemia |
from bad double stranded break without repair |
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benign tumors |
locally in invasion no penetration to basement membrane |
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malignant tumors |
invade tissues make metastases |
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source of carcinomas |
epithelial tissues |
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source os squamous cell carcinomas |
from epithelia of protective layer |
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adenocarcinomas |
from secretory epithelia |
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sarcomas |
from connective tissue (liposarcoma...) |
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is only one mutation sufficient for tumor development? |
no, at least 4 |
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somatic mutation |
de novo, passed in daughter cells, but not to next generations |
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germ line mutations |
in the sperm\egg\ gonads can be inhereted |
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proto oncogen |
if activated-> can cause cancer in genes that are responsible for the cell growth\ differentiation any mutation\ increased expression-> increased activity of cell-> proto oncogen-> oncogen e Myc, Ras, Src, HER2, |
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tumor suppressor genes |
their function is usually lost in cancer they "block" the growth and survivial of not so good cells some genes can also induce "fixing" of DNA p53, p16, Rb, APC, MLH1, MSH2, |
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what are the requests a cell must have in order to achiave "cancer mode" |
1. self sufficiency of GF 2. insensitivity to anti GF 3. tissue invading\ metastasis 4. limitless replications potentials 5. sustained angiogenesis 6. evading apoptotsis |
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in the abscence of GF\ presence of anti GF |
cells leave cell cycle and moves to G0 |
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TGF mutation |
are receptors -> cancer cells are insensitive to anti growth signals |
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senecense |
remain viable, but do not replicate (left the cell cycle phase) |
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philadelphia chromsome |
translocation of chromsome 9 and 22 leading to a fused chromsome and higher chances of CML |
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loss of EMT |
loss of epithelial gene expression -> cells migrate (metastases) |
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ras activation |
oncogenic blocks the hydrolysis of GTP and thus it is always active |
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raf kinase |
is rare when mutates it leads to malignant melanoma |
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transcription factors overexpression |
are difficult to inhibit since they are enzymes since thye bind to DNA -> if amplified ther are more copies of genes=> more copies of genes responsible for the division-> cancer n-myc = childhood neuroblastime also Burkitt's lymphoma (EBV+ malaria-> overexpression of nmyc) |
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stochastic model |
all tumor cells can proliferate and make new tumor cells |
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cancer stem cell model |
only a few cells can form new tumors |
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therapuatic viruses contains |
therapuetic genes and psi genes for packaging |
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helper virus contains |
genes for replication |
