ZEB2 Antibody [J21B10] | Primary Antibodies

Application: Reactivity: Human

Lane 1: HepG2, Lane 2: Hela, Lane 3: A549, Lane 4: K562

Usage Information

Dilution
WB1:2000-1:10000 IHC1:600-1:2400 IF1:250-1:1000

Application
WB, IHC, IF, ELISA

Reactivity
Human

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
136 kDa 140-150 kD
^*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
ZEB2 Antibody [J21B10] detects endogenous levels of total ZEB2 protein.

Clone
J21B10

Synonym(s)
Zinc finger E-box-binding homeobox 2; Smad-interacting protein 1; SMADIP1; Zinc finger homeobox protein 1b; ZEB2; KIAA0569; SIP1; ZFHX1B; ZFX1B

Background
ZEB2 belongs to the zinc finger E-box binding homeobox family of transcription factors and operates as a DNA-binding repressor with critical roles in development and cellular plasticity. It contains N-terminal and C-terminal zinc finger domains flanking a central homeodomain, enabling sequence-specific binding to E-box motifs (CAGGTG) and recruitment of corepressor complexes like CtBP and NuRD. ZEB2 interacts directly with phosphorylated R-SMAD2/3 downstream of TGF-β/BMP signaling, forming a complex that represses epithelial genes such as E-cadherin (CDH1), Crumbs3, and claudins while activating mesenchymal genes including N-cadherin, vimentin, fibronectin, and MMPs, to drive epithelial-mesenchymal transition. This repression occurs through chromatin remodeling via HDAC1/2 recruitment and histone deacetylation at target promoters, with ZEB2 also undergoing auto-regulatory feedback by binding its own promoter. ZEB2 coordinates neuroectoderm induction from BMP/Wnt signals, promotes neural crest delamination and migration by repressing Foxd3 and Sox10, and directs hippocampal and neocortical layering through radial glia specification. TGF-β-induced ZEB2 expression sustains EMT in migrating neural crest cells and trophoblast invasion, while in T cell differentiation, it enforces Th17 commitment via RORγt stabilization and IL-17 production. Post-translational SUMOylation at lysine residues enhances ZEB2 stability and activity, whereas miR-200 family members form a double-negative feedback loop to balance epithelial state. During injury repair, ZEB2 drives astrocyte proliferation and Schwann cell differentiation for remyelination via EMT programs. Haploinsufficiency causes Mowat-Wilson syndrome with neurodevelopmental defects, including Hirschsprung disease and intellectual disability, while overexpression correlates with poor prognosis in ovarian, colorectal, and melanoma through metastasis and stemness maintenance.

Background

ZEB2 belongs to the zinc finger E-box binding homeobox family of transcription factors and operates as a DNA-binding repressor with critical roles in development and cellular plasticity. It contains N-terminal and C-terminal zinc finger domains flanking a central homeodomain, enabling sequence-specific binding to E-box motifs (CAGGTG) and recruitment of corepressor complexes like CtBP and NuRD. ZEB2 interacts directly with phosphorylated R-SMAD2/3 downstream of TGF-β/BMP signaling, forming a complex that represses epithelial genes such as E-cadherin (CDH1), Crumbs3, and claudins while activating mesenchymal genes including N-cadherin, vimentin, fibronectin, and MMPs, to drive epithelial-mesenchymal transition. This repression occurs through chromatin remodeling via HDAC1/2 recruitment and histone deacetylation at target promoters, with ZEB2 also undergoing auto-regulatory feedback by binding its own promoter. ZEB2 coordinates neuroectoderm induction from BMP/Wnt signals, promotes neural crest delamination and migration by repressing Foxd3 and Sox10, and directs hippocampal and neocortical layering through radial glia specification. TGF-β-induced ZEB2 expression sustains EMT in migrating neural crest cells and trophoblast invasion, while in T cell differentiation, it enforces Th17 commitment via RORγt stabilization and IL-17 production. Post-translational SUMOylation at lysine residues enhances ZEB2 stability and activity, whereas miR-200 family members form a double-negative feedback loop to balance epithelial state. During injury repair, ZEB2 drives astrocyte proliferation and Schwann cell differentiation for remyelination via EMT programs. Haploinsufficiency causes Mowat-Wilson syndrome with neurodevelopmental defects, including Hirschsprung disease and intellectual disability, while overexpression correlates with poor prognosis in ovarian, colorectal, and melanoma through metastasis and stemness maintenance.

References
https://pubmed.ncbi.nlm.nih.gov/26193487/ https://pubmed.ncbi.nlm.nih.gov/30773635/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%