CXXC5 Antibody [L11K10] Datasheet

Biological Description

Specificity	CXXC5 Antibody [L11K10] detects endogenous levels of total CXXC5 protein.
Background	CXXC5 belongs to the CXXC-type zinc finger protein family that recognizes unmethylated CpG dinucleotides and modulates Wnt/β-catenin signaling alongside BMP and TGF-β pathways during development and differentiation. It consists of a central CXXC domain flanked by acidic and proline-rich regions that mediate DNA binding and protein-protein interactions with Dishevelled, Smad3/4, and transcriptional co-regulators. CXXC5 suppresses canonical Wnt signaling by sequestering Dishevelled through direct binding that prevents LRP5/6 phosphorylation and β-catenin stabilization, thereby repressing target gene activation like Runx2 during osteoblast commitment while promoting non-canonical planar cell polarity through selective Dvl2 engagement. CXXC5 facilitates BMP-induced endothelial differentiation by coordinating VEGFR2 transcription via Smad1/5/8 nuclear translocation and enhances TGF-β-mediated apoptosis through Smad3 phosphorylation and Smad4 nuclear import that drives pro-apoptotic gene sets. CXXC5 transcriptionally activates MyoD and myogenin promoters to drive C2C12 myoblast fusion and sarcomere assembly, integrating with retinoic acid signaling for lineage specification. CXXC5 governs myelopoiesis through cytokine-driven maturation of hematopoietic precursors and supports angiogenesis via endothelial migration on VEGF gradients, with peak expression in embryonic mesoderm and adult bone marrow reflecting stage-specific roles in tissue morphogenesis.

Specificity

CXXC5 Antibody [L11K10] detects endogenous levels of total CXXC5 protein.

Background

CXXC5 belongs to the CXXC-type zinc finger protein family that recognizes unmethylated CpG dinucleotides and modulates Wnt/β-catenin signaling alongside BMP and TGF-β pathways during development and differentiation. It consists of a central CXXC domain flanked by acidic and proline-rich regions that mediate DNA binding and protein-protein interactions with Dishevelled, Smad3/4, and transcriptional co-regulators. CXXC5 suppresses canonical Wnt signaling by sequestering Dishevelled through direct binding that prevents LRP5/6 phosphorylation and β-catenin stabilization, thereby repressing target gene activation like Runx2 during osteoblast commitment while promoting non-canonical planar cell polarity through selective Dvl2 engagement. CXXC5 facilitates BMP-induced endothelial differentiation by coordinating VEGFR2 transcription via Smad1/5/8 nuclear translocation and enhances TGF-β-mediated apoptosis through Smad3 phosphorylation and Smad4 nuclear import that drives pro-apoptotic gene sets. CXXC5 transcriptionally activates MyoD and myogenin promoters to drive C2C12 myoblast fusion and sarcomere assembly, integrating with retinoic acid signaling for lineage specification. CXXC5 governs myelopoiesis through cytokine-driven maturation of hematopoietic precursors and supports angiogenesis via endothelial migration on VEGF gradients, with peak expression in embryonic mesoderm and adult bone marrow reflecting stage-specific roles in tissue morphogenesis.

Usage Information

Application

WB, IP, IF

Dilution

WB	IP	IF
1:1000	1:100	1:1000

Reactivity

Human, Mouse, Rat, Monkey

Source

Rabbit Monoclonal Antibody

MW

33 kDa

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

References

https://pubmed.ncbi.nlm.nih.gov/29928427/
https://pubmed.ncbi.nlm.nih.gov/25633194/

Application Data

WB

Validated by Selleck

Lane 1: MCF7, Lane 2: T47D, Lane 3: COS, Lane 4: H-4-II-E