6 DNA damage p53 TNF Cell death.ppt
- Количество слайдов: 110
DNA Damage Signaling
DNA damage sensors DNA repair Cell cycle arrest (checkpoints activation) Apoptosis
PI 3 K-related protein kinases in DNA damage signaling ATM DNA-PK ATR
DNA damage sensing and signaling to cell cycle
DNA repair pathways by iniciation - Global Genomic Repair (GGR), including Replication-coupled repair (connected to stalled replication fork signaling, replicative stress signaling) - Transcription-coupled repair - Diferentiation-associated repair
DNA repair pathways by type of DNA damage Single-strand damage repair Double-strand damage repair
DNA repair pathways by type of DNA damage Double-strand damage repair Single-strand damage repair Mismatch repair Direct reversal Gap ligation Base excision repair Nucleotide excision repair
Base vs nucleotide excision repair
Excision repair pathways
Depurination and deamination
UV-induced pyrimidine dimers
Mammalian DNA damage sensors
Mammalian UV-induced DNA damage recognition
PARP in single-strand breaks repair
DNA damage sensing and signaling to cell cycle
ATR activation ATRIP — esssential regulatory subunit For activation reguires RPA (binds to ss. DNA) and TOPBP 1 (usually binds to Rad 9 -Rad 1 -Hus 1 complex detecting ss-ds. DNA border) Timeless and Tipin (Circadian clock proteins) and BRCA 1 needed for ATR activation or signaling. Activated in responce to: - NER - Stalled replication fork - Fanconi anemia pathway - ATM activation or strand resection in DSB (in S/G 2) - Mismatch repair (via Msh 2) Has functions in normal replication
ATM and ATR activation
ATR functions - cell cycle arrest (S, G 1, G 2) - preventing firing of late replication origins (Cdc 45 binding) 12 in S - ? prevention of lycenzing in G 1 (Cdt 1 degradation) - stabilizing stressed replication forks in S - promoting DNA repair and restart of replication - apoptosos induction - functions in normal replication
ATR substrates Rad 17, Claspin — for Chk 1 binding Chk 1 — for cell cycle arrest p 53 — for cell cycle arrest, apoptosis, repair Siah 1 — for HIPK 2 stabilisation to p 53 Hus 1, ATRIP, RPA, Top. BP 1 — feedback E 2 F 1 — for cell cycle arrest Cdc 7 -DBF 4, Mll 1 — blocking firing of later origins (also via Cdc 25) BRCA 1, Mdc 1, H 2 AX — usually by ATM for HR PLK (via Claspin and Mcm 2, for Chk 1 inactivation)
p. S/p. T recognision domains and proteins in DNA damage response BRCT domains (in BRCA 1, Top. BP 1, Mdc 1, Nbs 1, PARP 1, 53 BP 1) FHA domains (in Chk 2, Mdc 1, RNF 8) 14 -3 -3 proteins SCF Ub-ligases
HIPK 1 to p 53
Chk 1 substrates Cdc 25 A (degradation) — for cell cycle arrest Cdc 25 C (inactivation) — for cell cycle arrest Wee 1 p 53 — for cell cycle arrest, apoptosis, repair BRCA 2, Rad 51 — for HR
Transcription-coupled repair To NER — via CSA, CSB, XAB 2 To MMR — via Mlh 1, Msh 2 To BER — via CSA, CSB, BRCA 1
DNA repair pathways by type of DNA damage Single-strand damage Double-strand repair damage repair Classical non-homologous end jojning (c. NHEJ) Alternative Repair by non-homologous end jojning (a. NHEJ, MMEJ) recombination (HRR)
Double strain breaks repair
Double-strand damage - Double-strand breaks (competing pathways: Ku-DNA-PK (c. NHEJ) and PARP-ATM (HR, a. NHEJ) - RAG-induced breaks (i. e, V(D)J recombination) — c. NHEJ via DNA-PK - Stalled-replication fork-induced breaks - Single-strand to double-strand break conversion - Interstrand crosslinks (detection by Fanconi anemia pathway — first to ATR)
Pathways of DSB repair
c-NHEJ and DNA-PK Ku
HRR and PARP
ATM activation Mre 11 -Rad 50 -Nbs 1 complex binds DSB and activates ATM. Inactive dimeric ATM → trans-autophosphorylation → active monomeric ATM Activated in responce to double-strand breaks γH 2 AX, BRCA 1, Mdc 1, 53 BP 1 help in activation (positive feedback)
ATM and ATR activation
ATM substrates H 2 AX — for Mdc 1 and other binding Mdc 1 — for γH 2 AX spreading (interacts with Nbs 1 in MRN) and further complex formation Chk 2 — for cell cycle arrest (dimerisation via FHAdomain and autophosphorylation) 53 BP 1 — for p 53 binding (via γH 2 AX) Mdm 2, Mdm. X — for p 53 stabilisation p 53 — for cell cycle arrest, apoptosis, repair Siah 1 — for HIPK 2 stabilisation to p 53 BRCA 1, 2 — for HR (via γH 2 AX) Nbs 1 (MRN complex) Smc 1 (cohesin)
Signaling from γH 2 AX to BRCA 1 and BRCA 2 z
Chk 2 substrates Cdc 25 A (degradation) — for cell cycle arrest Cdc 25 C (inactivation) — for cell cycle arrest p 53 — for cell cycle arrest, apoptosis, repair Mdm. X — for p 53 stabilisation (Chk 2) BRCA 1 — for HR Fox. M 1, E 2 F 1
DNA damage sensing and signaling to cell cycle
p 53
DNA damage ROS, UV, hyperosmolarity ATM, ATR, DNA-PK, HIPK 2 JNK, p 38, MK 2 Too strong proliferation Mdm 2 p 53 stabilisation and activation Apoptosis Autophagy Cell cycle arrest Senescence Other, including DNA repair
p 53 response to DNA damage
Phosphorylation of p 53
Phosphorylation of p 53
Phosphorylation of p 53 (continued)
HIPK 1 to p 53
Acetylation of p 53
Other regulators of p 53
Cell cycle dependent p 53 induction E 2 F-1 p 19 ARF mdm 2 p 53 p 21 waf Cy/cdk
p 53/MDM-2/p 19 ARF feedback loop
DNA excision repair proteins induced by p 53 - p 48/DDB 2 (XPE/UV-DDB component) - XPC - GADD 45
p 53 and cell cycle regulation
p 53 and apoptosis
p 53 and apoptosis
p 53, oncogenic transformation and the decision between life and death
Other functions - Inhibits angiogenesis (thrombospondin expression) - Inhibits glycolysis (TIGAR), promotes oxidative phosphorylation (SCO 2) - Stimulates embrio implantation (LIF expression) -Pro- or antioxidative features
Pro- and antioxidant functions of p 53 regulated by acetylation
c-Abl and p 73
TNFR-family and IL-1 R-family receptors
TNFR-family Death Domaincontaining (Fas, TNFR 1, DR 3, DR 4, DR 5) Activation of caspase 8 (and 10), pro-apoptotic IL-1 R-family (IL-1, IL-18, TLR) Without Death Domains (TNFR 2, CD 27, CD 30, CD 40, Ox 40, LTβR) Activation of NFκB and JNK, anti-apoptotic
TNF family
Fas. L, TNF and Apo 3 L/TWEAK signaling
TRIAL signaling and decoy receptors
Direct interactions between TRAFs and TNF R-family receptors
Interactions between TRAFs and other intracellular proteins
NF B activation TAK TNF-fam. , IL-1 fam. , stress factors NIK MEKK 1 (NF B-inducing kinase) Ik. B NLS NF B
NFk. B activation
NFk. B activation
IL 1 R family
Toll-like receptors
Apoptosis
He. La, etoposide 2. 5 mk. M Blue – DAPI Green – cytochrome c Red – active caspase 3
Caspases
Apoptotic caspases Initiatory – caspases 8 (and 10), 9, 2, 12(? ) Executive – caspases 3, 7 and 6
The two pathways for caspase activation
The two pathways for caspase activation
Bcl-2 family proteins in the regulation of cytochrom c release
Bcl-2 family
Mitochondrial permeability transition
Mitochondrial permeability transition
Mitochondrial intermembrane protein release
Mitochondrial intermembrane protein release
Some inhibitors of caspase activation - IAPs (IAP 1, 2, survivin, XIAP) (for caspase 9) -FLIP, BAR, ARC (for caspase 8)
Some more important apoptosis inducers -Caspase 2 -Nuclear Daxx -Nur 77 -p 73 -Ceramide and sphingosine
Caspase 2 in apoptosis p 53 TNFR-family PIDD RIP, TRADD RAIDD Pro-caspase 2 Caspase 2
Some more apoptosis inducers -Caspase 2 -Nuclear Daxx -Nur 77 -p 73 -Ceramide and sphingosine
Ceramide and sphingosine
Ceramide and sphingosine
Ceramide in apoptosis
Apoptotic ceramide targets
Non-apoptotic cell death
Non-apoptotic cell death variants - Caspase-independent apoptosis-like processes - Autophagy (type II programmed cell death) - Necrosis - Mitotic catastrophe
Autophagy
Autophagy and apoptosis
Signaling to autophagy
Signaling to autophagy
Signaling to autophagy -(PKR) e. IF 2α -GAIP (GAP for Gαi 3) -BNIP 3 both apoptosis and autophagy -DAPK, DRP 1 - PI 3 K-PKB-m. Tor inhibits - AMPK (inhibits m. TOR) - Beclin 1 (activates Class III PI 3 K, inhibited by Bcl-2/Blc. XL)
NO and apoptosis-to-necrosis switch
Mitotic catastrophe U 1810, etoposide 2. 5 Blue – DAPI Green – Ran
He. La, etoposide 2. 5 mk. M Blue – DAPI Green – cytochrome c Red – active caspase 3