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NF-κB Signaling Dynamics

A delayed negative-feedback circuit that turns a steady signal into oscillations.

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NF-κB is an inflammatory transcription factor that is normally kept inactive in the cytoplasm by IκB proteins. When a stimulus (IKK) arrives, it triggers degradation of IκB, freeing NF-κB to switch on and enter the nucleus. But NF-κB also drives synthesis of new IκB — a negative feedback loop that eventually shuts it back off. Because making new IκB (transcription, translation, and folding) takes time — a delay τ — the system overshoots before the brakes kick in, producing sustained oscillations rather than settling smoothly. This model includes two such feedback loops: a fast one (IκBα) and a slow one (IκBε). Drag τ and the IKK stimulus strength, or click the amplitude map, to see how the oscillations change.

Reaction network

(R1)NFκB+IkBαkaNFκB:IkBα(R2)NFκB:IkBαkdNFκB+IkBα(R3)IKK+NFκB:IkBαrIKK+NFκB(R4)IKK+IkBαrIKK(R5)IkBαg(R6)NFκB+prIkBαfaNFκB:prIkBα(R7)NFκB:prIkBαfdNFκB+prIkBα(R8)prIkBαa1prIkBα+IkBα(R9)NFκB:prIkBαb1NFκB:prIkBα+IkBα(R10)NFκB+IkBεkaNFκB:IkBε(R11)NFκB:IkBεkdNFκB+IkBε(R12)IKK+NFκB:IkBεrIKK+NFκB(R13)IKK+IkBεrIKK(R14)IkBεg(R15)NFκB+prIkBεfaNFκB:prIkBε(R16)NFκB:prIkBεfdNFκB+prIkBε(R17)prIkBεa2prIkBε+IkBε(R18)NFκB:prIkBεb2NFκB:prIkBε+IkBε\begin{array}{rlcl} (\text{R1}) & \text{NF}\kappa\text{B} + \text{IkB}_\alpha & \xrightarrow{k_a} & \text{NF}\kappa\text{B}{:}\text{IkB}_\alpha \\[3pt] (\text{R2}) & \text{NF}\kappa\text{B}{:}\text{IkB}_\alpha & \xrightarrow{k_d} & \text{NF}\kappa\text{B} + \text{IkB}_\alpha \\[3pt] (\text{R3}) & \text{IKK} + \text{NF}\kappa\text{B}{:}\text{IkB}_\alpha & \xrightarrow{r} & \text{IKK} + \text{NF}\kappa\text{B} \\[3pt] (\text{R4}) & \text{IKK} + \text{IkB}_\alpha & \xrightarrow{r} & \text{IKK} \\[3pt] (\text{R5}) & \text{IkB}_\alpha & \xrightarrow{g} & \varnothing \\[3pt] (\text{R6}) & \text{NF}\kappa\text{B} + \text{prIkB}_\alpha & \xrightarrow{f_a} & \text{NF}\kappa\text{B}{:}\text{prIkB}_\alpha \\[3pt] (\text{R7}) & \text{NF}\kappa\text{B}{:}\text{prIkB}_\alpha & \xrightarrow{f_d} & \text{NF}\kappa\text{B} + \text{prIkB}_\alpha \\[3pt] (\text{R8}) & \text{prIkB}_\alpha & \xrightarrow{a_1} & \text{prIkB}_\alpha + \text{IkB}_\alpha \\[3pt] (\text{R9}) & \text{NF}\kappa\text{B}{:}\text{prIkB}_\alpha & \xrightarrow{b_1} & \text{NF}\kappa\text{B}{:}\text{prIkB}_\alpha + \text{IkB}_\alpha \\[3pt] (\text{R10}) & \text{NF}\kappa\text{B} + \text{IkB}_\varepsilon & \xrightarrow{k_a} & \text{NF}\kappa\text{B}{:}\text{IkB}_\varepsilon \\[3pt] (\text{R11}) & \text{NF}\kappa\text{B}{:}\text{IkB}_\varepsilon & \xrightarrow{k_d} & \text{NF}\kappa\text{B} + \text{IkB}_\varepsilon \\[3pt] (\text{R12}) & \text{IKK} + \text{NF}\kappa\text{B}{:}\text{IkB}_\varepsilon & \xrightarrow{r} & \text{IKK} + \text{NF}\kappa\text{B} \\[3pt] (\text{R13}) & \text{IKK} + \text{IkB}_\varepsilon & \xrightarrow{r} & \text{IKK} \\[3pt] (\text{R14}) & \text{IkB}_\varepsilon & \xrightarrow{g} & \varnothing \\[3pt] (\text{R15}) & \text{NF}\kappa\text{B} + \text{prIkB}_\varepsilon & \xrightarrow{f_a} & \text{NF}\kappa\text{B}{:}\text{prIkB}_\varepsilon \\[3pt] (\text{R16}) & \text{NF}\kappa\text{B}{:}\text{prIkB}_\varepsilon & \xrightarrow{f_d} & \text{NF}\kappa\text{B} + \text{prIkB}_\varepsilon \\[3pt] (\text{R17}) & \text{prIkB}_\varepsilon & \xrightarrow{a_2} & \text{prIkB}_\varepsilon + \text{IkB}_\varepsilon \\[3pt] (\text{R18}) & \text{NF}\kappa\text{B}{:}\text{prIkB}_\varepsilon & \xrightarrow{b_2} & \text{NF}\kappa\text{B}{:}\text{prIkB}_\varepsilon + \text{IkB}_\varepsilon \end{array}

These 18 mass-action reactions define the system, and each becomes a term in the 9 coupled ODEs. The two feedback loops are identical in form — α (R1–R9) and ε (R10–R18) — but differ in speed. The IκB synthesis reactions (R8, R9 and R17, R18) are the ones that carry the transcriptional delay τ: new IκB appears only τ minutes after NF-κB binds the promoter, and that lag is what turns steady signaling into oscillations. The stiff system is integrated with an adaptive Runge–Kutta (Dormand–Prince) solver.

Ordinary differential equations

d[NFκB]dt=kaNFκBIκBα+kdNFκB:IκBα+rIKKNFκB:IκBαkaNFκBIκBε+kdNFκB:IκBε+rIKKNFκB:IκBεfaNFκBprIκBα+fdNFκB:prIκBαfaNFκBprIκBε+fdNFκB:prIκBεd[IκBα]dt=kaNFκBIκBα+kdNFκB:IκBα+a1prIκBα(tτ)+b1NFκB:prIκBα(tτ)gIκBαrIKKIκBαd[IκBε]dt=kaNFκBIκBε+kdNFκB:IκBε+a2prIκBε(tτ)+b2NFκB:prIκBε(tτ)gIκBεrIKKIκBεd[NFκB:IκBα]dt=kaNFκBIκBαkdNFκB:IκBαrIKKNFκB:IκBαd[NFκB:IκBε]dt=kaNFκBIκBεkdNFκB:IκBεrIKKNFκB:IκBεd[prIκBα]dt=faNFκBprIκBα+fdNFκB:prIκBαd[prIκBε]dt=faNFκBprIκBε+fdNFκB:prIκBεd[NFκB:prIκBα]dt=faNFκBprIκBαfdNFκB:prIκBαd[NFκB:prIκBε]dt=faNFκBprIκBεfdNFκB:prIκBε\small \def\N{\text{NF}\kappa\text{B}} \def\Aa{\text{I}\kappa\text{B}_\alpha} \def\Ae{\text{I}\kappa\text{B}_\varepsilon} \def\Ca{\N{:}\Aa} \def\Ce{\N{:}\Ae} \def\Pa{\text{prI}\kappa\text{B}_\alpha} \def\Pe{\text{prI}\kappa\text{B}_\varepsilon} \def\Qa{\N{:}\Pa} \def\Qe{\N{:}\Pe} \def\IKK{\text{IKK}} \begin{aligned} \frac{d[\N]}{dt} ={}& -k_a\,\N\,\Aa + k_d\,\Ca + r\,\IKK\,\Ca - k_a\,\N\,\Ae + k_d\,\Ce + r\,\IKK\,\Ce \\ &{} - f_a\,\N\,\Pa + f_d\,\Qa - f_a\,\N\,\Pe + f_d\,\Qe \\[6pt] \frac{d[\Aa]}{dt} ={}& -k_a\,\N\,\Aa + k_d\,\Ca + \textcolor{#d97706}{a_1\,\Pa(t-\tau) + b_1\,\Qa(t-\tau)} - g\,\Aa - r\,\IKK\,\Aa \\[6pt] \frac{d[\Ae]}{dt} ={}& -k_a\,\N\,\Ae + k_d\,\Ce + \textcolor{#10b981}{a_2\,\Pe(t-\tau) + b_2\,\Qe(t-\tau)} - g\,\Ae - r\,\IKK\,\Ae \\[6pt] \frac{d[\Ca]}{dt} ={}& k_a\,\N\,\Aa - k_d\,\Ca - r\,\IKK\,\Ca \\[6pt] \frac{d[\Ce]}{dt} ={}& k_a\,\N\,\Ae - k_d\,\Ce - r\,\IKK\,\Ce \\[6pt] \frac{d[\Pa]}{dt} ={}& -f_a\,\N\,\Pa + f_d\,\Qa \\[6pt] \frac{d[\Pe]}{dt} ={}& -f_a\,\N\,\Pe + f_d\,\Qe \\[6pt] \frac{d[\Qa]}{dt} ={}& f_a\,\N\,\Pa - f_d\,\Qa \\[6pt] \frac{d[\Qe]}{dt} ={}& f_a\,\N\,\Pe - f_d\,\Qe \end{aligned}

The colored terms are the delayed IκB synthesis (α and ε loops) that carry the τ delay.

Full species list
  • NF-κB (free, active)
  • IκBα (free)
  • NF-κB:IκBα complex
  • IκBα promoter (transcribing)
  • NF-κB:IκBα-promoter complex
  • IκBε (free)
  • NF-κB:IκBε complex
  • IκBε promoter (transcribing)
  • NF-κB:IκBε-promoter complex