IκB-ζ Antibody [K24D5] | Primary Antibodies

Application: Reactivity: Mouse

Usage Information

Dilution
WB1:1000 IP1:50 CHIP1:50

Application
WB, IP, ChIP

Reactivity
Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
78 kDa 75 kDa, 85 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
IκB-ζ Antibody [K24D5] detects endogenous levels of total IκB-ζ protein.

Clone
K24D5

Synonym(s)
AA408868, I-kappa-B-zeta, IkappaB-zeta, IkappaBzeta, IkB-zeta, IKBZ, IL-1 inducible nuclear ankyrin-repeat protein, INAP, MAIL, Molecule possessing ankyrin repeats induced by lipopolysaccharide, OTTMUSP00000021591, OTTMUSP00000021593.

Background
IκB-ζ (also known as MAIL/INAP) is an atypical member of the IκB family encoded by NFKBIZ, functionally positioned as a nuclear transcriptional regulator that integrates Toll-like receptor and interleukin-1 receptor signaling with selective NF-κB–dependent gene expression in immune and barrier tissues. IκB-ζ contains a C-terminal array of ankyrin repeats that binds preferentially to NF-κB subunits such as p50 and p52, while its N-terminal regulatory region accommodates phosphorylation and interaction motifs that modulate its stability and transcriptional regulatory capacity in response to upstream signals. IκB-ζ expression is induced downstream of MyD88-dependent TLR and IL-1R pathways via an IRAK1/IRAK4- and TRAF6-dependent module that promotes NF-κB–mediated Nfkbiz transcription and a distinct post-transcriptional mechanism that acts through a defined regulatory element in the IκB-ζ mRNA to enhance message accumulation in activated macrophages and other innate immune cells. IκB-ζ associates with NF-κB complexes on κB-containing promoters and functions as a transcriptional co-regulator that enables the induction of a subset of secondary response genes, including proinflammatory mediators such as interleukin-6 and other late-phase NF-κB targets, while repressing or attenuating expression of a different subset of NF-κB-responsive genes, thereby shaping promoter- and context-specific transcriptional outputs and establishing a differential gene expression profile downstream of common upstream cues. Within B cells, IκB-ζ induction follows engagement of the B-cell receptor and TLRs and depends on NF-κB–driven transcription combined with mRNA stabilization, and IκB-ζ supports expression of immunoregulatory genes such as IL-10 and CTLA4, contributes to optimal proliferative responses, and constrains surface costimulatory molecule upregulation under TLR stimulation, indicating a role in balancing activation and tolerance in adaptive immune compartments. IκB-ζ operates as a central node in inflammatory signaling by acting at the chromatin level as a cofactor for NF-κB on specific promoters, by integrating parallel signaling inputs that control its transcription and mRNA stability, and by imposing temporal control over inflammatory gene networks in macrophages, epithelial cells, and B cells, which makes it a critical determinant of how cells respond to persistent or combined innate and adaptive stimuli. Dysregulated IκB-ζ expression or function contributes to chronic inflammatory states and cancer, where constitutive NF-κB activity in certain lymphoma or solid tumor contexts depends on IκB-ζ to sustain a pathogenic transcriptional program, and where increased or ectopic IκB-ζ levels correlate with enhanced survival, inflammatory mediator production, or altered tissue homeostasis.

Background

IκB-ζ (also known as MAIL/INAP) is an atypical member of the IκB family encoded by NFKBIZ, functionally positioned as a nuclear transcriptional regulator that integrates Toll-like receptor and interleukin-1 receptor signaling with selective NF-κB–dependent gene expression in immune and barrier tissues. IκB-ζ contains a C-terminal array of ankyrin repeats that binds preferentially to NF-κB subunits such as p50 and p52, while its N-terminal regulatory region accommodates phosphorylation and interaction motifs that modulate its stability and transcriptional regulatory capacity in response to upstream signals. IκB-ζ expression is induced downstream of MyD88-dependent TLR and IL-1R pathways via an IRAK1/IRAK4- and TRAF6-dependent module that promotes NF-κB–mediated Nfkbiz transcription and a distinct post-transcriptional mechanism that acts through a defined regulatory element in the IκB-ζ mRNA to enhance message accumulation in activated macrophages and other innate immune cells. IκB-ζ associates with NF-κB complexes on κB-containing promoters and functions as a transcriptional co-regulator that enables the induction of a subset of secondary response genes, including proinflammatory mediators such as interleukin-6 and other late-phase NF-κB targets, while repressing or attenuating expression of a different subset of NF-κB-responsive genes, thereby shaping promoter- and context-specific transcriptional outputs and establishing a differential gene expression profile downstream of common upstream cues. Within B cells, IκB-ζ induction follows engagement of the B-cell receptor and TLRs and depends on NF-κB–driven transcription combined with mRNA stabilization, and IκB-ζ supports expression of immunoregulatory genes such as IL-10 and CTLA4, contributes to optimal proliferative responses, and constrains surface costimulatory molecule upregulation under TLR stimulation, indicating a role in balancing activation and tolerance in adaptive immune compartments. IκB-ζ operates as a central node in inflammatory signaling by acting at the chromatin level as a cofactor for NF-κB on specific promoters, by integrating parallel signaling inputs that control its transcription and mRNA stability, and by imposing temporal control over inflammatory gene networks in macrophages, epithelial cells, and B cells, which makes it a critical determinant of how cells respond to persistent or combined innate and adaptive stimuli. Dysregulated IκB-ζ expression or function contributes to chronic inflammatory states and cancer, where constitutive NF-κB activity in certain lymphoma or solid tumor contexts depends on IκB-ζ to sustain a pathogenic transcriptional program, and where increased or ectopic IκB-ζ levels correlate with enhanced survival, inflammatory mediator production, or altered tissue homeostasis.

References
https://pubmed.ncbi.nlm.nih.gov/23728777/ https://pubmed.ncbi.nlm.nih.gov/17447895/

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%