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Difference between revisions of "Template:SUIT-017"

From Bioblast
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| [[Fatty acid oxidation pathway control state| F(N)]]
| [[Fatty acid oxidation pathway control state| F(N)]]
| FAO
| FAO
| OctM<sub>''L''</sub> or OctM_L: Octanoylcarnitine & low malate, N-LEAK respiration, N<sub>''L''</sub>
| 1OctM


{{Template:SUIT F}} {{Template:SUIT M low}} {{Template: SUIT L(n)}}
{{Template:SUIT F}} {{Template:SUIT M low}} {{Template: SUIT L(n)}}
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| [[FN]]
| [[FN]]
| F&CI
| F&CI
| 1OctM;2D;3G;
| 1OctM;2D;3G


{{Template:SUIT N}} {{Template:SUIT F}} {{Template:SUIT OXPHOS}}  
{{Template:SUIT N}} {{Template:SUIT F}} {{Template:SUIT OXPHOS}}  
|-
| 3c
| [[OctGM]]c<sub>''P''</sub>
| [[FN]]
| FAO
| 1OCtM;2D;3G;3c
{{Template:SUIT N}} {{Template:SUIT F}} {{Template:SUIT OXPHOS}} {{Template:SUIT c}}


|-
|-
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| [[FNS]]
| [[FNS]]
| F&CI&II
| F&CI&II
| 1OctM;2D;3G;3c;4S
| 1OctM;2D;3G;4S


{{Template:SUIT NS}} {{Template:SUIT F}} {{Template:SUIT OXPHOS}}
{{Template:SUIT NS}} {{Template:SUIT F}} {{Template:SUIT OXPHOS}}
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| [[FNS]]
| [[FNS]]
| F&CI&II
| F&CI&II
| 1OctM;2D;3G;3c;4S;5U
| 1OctM;2D;3G;4S;5U


{{Template:SUIT NS}} {{Template:SUIT F}} {{Template:SUIT ET}}
{{Template:SUIT NS}} {{Template:SUIT F}} {{Template:SUIT ET}}
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| [[S]]
| [[S]]
| CII
| CII
| 1OctM;2D;3G;3c;4S;5U;6Rot
| 1OctM;2D;3G;4S;5U;6Rot


{{Template:SUIT Rot}} {{Template:SUIT ET}}
{{Template:SUIT Rot}} {{Template:SUIT ET}}
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|
|
|  
|  
|  1OctM;2D;3G;3c;4S;5U;6Rot;7Ama
|  1OctM;2D;3G;4S;5U;6Rot;7Ama
{{Template:SUIT ROX}}
{{Template:SUIT ROX}}


|}
|}
{{Template:Keywords in SUIT protocols}}
{{Template:Keywords in SUIT protocols}}

Revision as of 18:17, 26 February 2019

MitoPedia: SUIT

Steps and respiratory states

1OctM;2D;2c;3G;4S;5U;6Rot;7Ama.png

Step State Pathway Q-junction Comment - Events (E) and Marks (M)
1OctM OctML F(N) FAO 1OctM

Respiratory stimulation of the FAO-pathway, F, by fatty acid, FA, in the presence of malate, M. Malate is a type N substrate (N), required for the F-pathway. The FA concentration has to be optimized to saturate the F-pathway, without inhibiting or uncoupling respiration. Low concentration of malate, typically 0.1 mM, does not saturate the N-pathway; but saturates the F-pathway. Non-phosphorylating resting state (LEAK state); LEAK respiration L(n) in the absence of ADP, ATP, AMP (no adenylates).

2D OctMP F(N) FAO 1OctM;2D

Respiratory stimulation of the FAO-pathway, F, by fatty acid, FA, in the presence of malate, M. Malate is a type N substrate (N), required for the F-pathway. The FA concentration has to be optimized to saturate the F-pathway, without inhibiting or uncoupling respiration. Low concentration of malate, typically 0.1 mM, does not saturate the N-pathway; but saturates the F-pathway. OXPHOS capacity P (with saturating [ADP]), active OXPHOS state.

3G OctGMP FN F&CI 1OctM;2D;3G

NADH-linked substrates (type N-pathway to Q). Respiratory stimulation of the FAO-pathway, F, by fatty acid, FA, in the presence of malate, M. Malate is a type N substrate (N), required for the F-pathway. The FA concentration has to be optimized to saturate the F-pathway, without inhibiting or uncoupling respiration. OXPHOS capacity P (with saturating [ADP]), active OXPHOS state.

4S OctGMSP FNS F&CI&II 1OctM;2D;3G;4S

Respiratory stimulation by simultaneous action of type N substrates & succinate, with convergent electron flow in the NS-pathway for reconstitution of TCA cycle function. Respiratory stimulation of the FAO-pathway, F, by fatty acid, FA, in the presence of malate, M. Malate is a type N substrate (N), required for the F-pathway. The FA concentration has to be optimized to saturate the F-pathway, without inhibiting or uncoupling respiration. OXPHOS capacity P (with saturating [ADP]), active OXPHOS state.

5U OctGMSE FNS F&CI&II 1OctM;2D;3G;4S;5U

Respiratory stimulation by simultaneous action of type N substrates & succinate, with convergent electron flow in the NS-pathway for reconstitution of TCA cycle function. Respiratory stimulation of the FAO-pathway, F, by fatty acid, FA, in the presence of malate, M. Malate is a type N substrate (N), required for the F-pathway. The FA concentration has to be optimized to saturate the F-pathway, without inhibiting or uncoupling respiration. Noncoupled electron transfer state, ET state, with ET capacity E.

6Rot SE S CII 1OctM;2D;3G;4S;5U;6Rot

Succinate pathway control state (S-pathway) after inhibiting CI with rotenone, which also inhibits the F-pathway. Noncoupled electron transfer state, ET state, with ET capacity E.

7Ama ROX 1OctM;2D;3G;4S;5U;6Rot;7Ama

Rox is the residual oxygen consumption in the ROX state, due to oxidative side reactions, estimated either after inhibition of CIII (e.g. antimycin A, myxothiazol), CIV (e.g. Cyanide) or in the absence of endogenous fuel-substrates. Rox is subtracted from oxygen flux as a baseline for all respiratory states, to obtain mitochondrial respiration.


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