Source 1review2009Annual Review of Immunology
Toolkit/Rel/NF-κB family of transcription factors
Rel/NF-κB family of transcription factors
Also known as: NF-κB family, Rel/NF-kappaB family
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The Rel/NF-κB family is a mammalian set of transcription factors comprising RelA, c-Rel, RelB, NF-κB1 (p50 and precursor p105), and NF-κB2 (p52 and precursor p100). These factors are differentially activated as NF-κB heterodimers by signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines to regulate transcription.
Usefulness & Problems
Why this is useful
This family is useful as a central transcriptional control module linking immune receptor signaling to gene expression. The cited literature specifically associates Rel/NF-κB activity with lymphocyte and lymphoid organ development, immune response control, and malignant transformation.
Source:
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
Problem solved
Rel/NF-κB factors solve the biological problem of converting diverse extracellular immune and inflammatory inputs into transcriptional responses. The evidence supports this role for signals from antigen receptors, pattern-recognition receptors, and TNF- and IL-1-family cytokine receptors.
Problem links
Need tighter control over gene expression timing or amplitude
DerivedThe Rel/NF-κB family comprises mammalian transcription factors including RelA, c-Rel, RelB, NF-κB1 (p50 and precursor p105), and NF-κB2 (p52 and precursor p100). These factors are differentially activated as NF-κB heterodimers by signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines to regulate transcription.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level protein part used inside a larger architecture that realizes a mechanism.
Mechanisms
HeterodimerizationHeterodimerizationHeterodimerizationtranscriptional regulationtranscriptional regulationTechniques
No technique tags yet.
Target processes
transcriptionImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: multi component delivery burdenoperating role: regulatorswitch architecture: multi componentswitch architecture: recruitment
The evidence identifies the relevant mammalian family members as RelA, c-Rel, RelB, NF-κB1/p50/p105, and NF-κB2/p52/p100. Beyond family composition and activation by immune receptor pathways, the supplied sources do not specify construct design, cofactors, delivery methods, or expression systems.
The supplied evidence describes endogenous biological roles rather than engineered performance characteristics of a tool. It does not provide construct-level implementation details, quantitative activity data, domain boundaries, or validation in synthetic biology applications.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
Approval Evidence
1 source4 linked approval claimsfirst-pass slug rel-nf-b-family-of-transcription-factors
The mammalian Rel/NF-kappaB family of transcription factors, including RelA, c-Rel, RelB, NF-kappaB1 (p50 and its precursor p105), and NF-kappaB2 (p52 and its precursor p100)...
Source:
activation inputsupports
Signals from antigen receptors, pattern-recognition receptors, and receptors for TNF and IL-1 family cytokines induce differential activation of NF-κB heterodimers.
A wide variety of signals emanating from antigen receptors, pattern-recognition receptors, receptors for the members of TNF and IL-1 cytokine families, and others induce differential activation of NF-kappaB heterodimers.
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biological process rolesupports
NF-κB family transcription factors regulate development and survival of lymphocytes and lymphoid organs, control of immune responses, and malignant transformation.
plays a central role in the immune system by regulating several processes ranging from the development and survival of lymphocytes and lymphoid organs to the control of immune responses and malignant transformation
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functional rolesupports
The mammalian Rel/NF-κB family of transcription factors plays a central role in the immune system.
The mammalian Rel/NF-kappaB family of transcription factors ... plays a central role in the immune system
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regulatory mechanismsupports
NF-κB family members are normally kept inactive in the cytoplasm by interaction with IkappaBs or with the unprocessed forms of NF-kappaB1 and NF-kappaB2.
The five members of the NF-kappaB family are normally kept inactive in the cytoplasm by interaction with inhibitors called IkappaBs or the unprocessed forms of NF-kappaB1 and NF-kappaB2.
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Comparisons
Source-backed strengths
A key strength is that multiple upstream receptor classes converge on NF-κB heterodimer activation, indicating broad integration of immune signaling inputs. The cited review also supports major physiological relevance in lymphocyte survival and development, immune regulation, and malignant transformation.
Compared with basic helix-loop-helix (bHLH) domain
Rel/NF-κB family of transcription factors and basic helix-loop-helix (bHLH) domain address a similar problem space because they share transcription.
Shared frame: same top-level item type; shared target processes: transcription; shared mechanisms: heterodimerization
Relative tradeoffs: looks easier to implement in practice.
Compared with HY5
Rel/NF-κB family of transcription factors and HY5 address a similar problem space because they share transcription.
Shared frame: same top-level item type; shared target processes: transcription; shared mechanisms: transcriptional regulation
Relative tradeoffs: appears more independently replicated; looks easier to implement in practice.
Compared with Q-PAS1
Rel/NF-κB family of transcription factors and Q-PAS1 address a similar problem space because they share transcription.
Shared frame: same top-level item type; shared target processes: transcription; shared mechanisms: heterodimerization
Relative tradeoffs: looks easier to implement in practice.
Ranked Citations
- 1.