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Mouse Anti-AXIN2 Recombinant Antibody (354214) (CBMAB-1177-CN)

This product is a rabbit antibody that recognizes AXIN2 of human. The antibody EPR2005(2) can be used for immunoassay techniques such as: IF, IHC-P, WB.
See all AXIN2 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
354214
Antibody Isotype
IgG1
Application
ICC

Basic Information

Immunogen
E. coli-derived recombinant human Axin-2 (Tyr550-Gln760).
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
IF(ICC)8-25 µg/ml

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Lyophilized
Buffer
PBS, Trehalose
Preservative
None
Concentration
2.274 - 2.43 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
axin 2
Introduction
The Axin-related protein, Axin2, presumably plays an important role in the regulation of the stability of beta-catenin in the Wnt signaling pathway, like its rodent homologs, mouse conductin/rat axil. In mouse, conductin organizes a multiprotein complex of APC (adenomatous polyposis of the colon), beta-catenin, glycogen synthase kinase 3-beta, and conductin, which leads to the degradation of beta-catenin. This protein acts as the inhibitor of the Wnt signaling pathway. It probably facilitates the phosphorylation of beta-catenin and APC by GSK3B.
Entrez Gene ID
Human8313
Mouse12006
Rat29134
Pig100739604
UniProt ID
HumanQ9Y2T1
MouseO88566
RatO70240
PigA0A287BFQ6
Alternative Names
AXIL; ODCRCS
Function
Inhibitor of the Wnt signaling pathway. Down-regulates beta-catenin. Probably facilitate the phosphorylation of beta-catenin and APC by GSK3B.
Biological Process
Beta-catenin-TCF complex assembly Source: Reactome
Bone mineralization Source: Ensembl
Cell population proliferation Source: Ensembl
Cellular protein localization Source: BHF-UCL
Chondrocyte differentiation involved in endochondral bone morphogenesis Source: Ensembl
Intramembranous ossification Source: Ensembl
Maintenance of DNA repeat elements Source: BHF-UCL
mRNA stabilization Source: BHF-UCL
Negative regulation of canonical Wnt signaling pathway Source: BHF-UCL
Negative regulation of cell population proliferation Source: BHF-UCL
Negative regulation of osteoblast differentiation Source: Ensembl
Odontogenesis Source: BHF-UCL
Positive regulation of canonical Wnt signaling pathway Source: Reactome
Positive regulation of cell death Source: BHF-UCL
Positive regulation of epithelial to mesenchymal transition Source: BHF-UCL
Positive regulation of protein phosphorylation Source: BHF-UCL
Regulation of centromeric sister chromatid cohesion Source: BHF-UCL
Regulation of chondrocyte development Source: Ensembl
Regulation of mismatch repair Source: BHF-UCL
Secondary heart field specification Source: Ensembl
Somitogenesis Source: Ensembl
Wnt signaling pathway Source: UniProtKB-KW
Cellular Location
Cytoplasm
Involvement in disease
Colorectal cancer (CRC): A complex disease characterized by malignant lesions arising from the inner wall of the large intestine (the colon) and the rectum. Genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Risk factors for cancer of the colon and rectum include colon polyps, long-standing ulcerative colitis, and genetic family history.
Oligodontia-colorectal cancer syndrome (ODCRCS): Affected individuals manifest severe tooth agenesis and colorectal cancer or precancerous lesions of variable types.
PTM
Probably phosphorylated by GSK3B and dephosphorylated by PP2A.
ADP-ribosylated by tankyrase TNKS and TNKS2. Poly-ADP-ribosylated protein is recognized by RNF146, followed by ubiquitination and subsequent activation of the Wnt signaling pathway.
Ubiquitinated by RNF146 when poly-ADP-ribosylated, leading to its degradation and subsequent activation of the Wnt signaling pathway. Deubiquitinated by USP34, deubiquitinated downstream of beta-catenin stabilization step: deubiquitination is important Wnt signaling to positively regulate beta-catenin (CTNBB1)-mediated transcription.

Niu, Z., Wang, F., Lv, S., Lv, Y., Liu, M., Fu, L., ... & Yuan, F. (2021). HNRNPU-AS1 regulates cell proliferation and apoptosis via miR-205-5p/AXIN2 axis and Wnt/β-catenin signaling pathway in cervical cancer. Molecular and Cellular Biology, MCB-00115.

Li, X., Li, Y., Liu, G., & Wu, W. (2021). New insights of the correlation between AXIN2 polymorphism and cancer risk and susceptibility: evidence from 72 studies. BMC cancer, 21(1), 1-15.

Kaur, G., Verma, R., Mukhopadhyay, C. S., & Sethi, R. (2021). Elevated pulmonary levels of Axin2 in mice exposed to herbicide 2, 4‐D with or without endotoxin. Journal of Biochemical and Molecular Toxicology, e22912.

Moshkovsky, A. R., & Kirschner, M. W. (2021). The non-redundant nature of the Axin2 regulatory network in the canonical Wnt signaling pathway. bioRxiv.

Cavallo, J. C., Scholpp, S., & Flegg, M. B. (2020). Delay-driven oscillations via Axin2 feedback in the Wnt/β-catenin signalling pathway. Journal of Theoretical Biology, 507, 110458.

Bernkopf, D. B., Brückner, M., Hadjihannas, M. V., & Behrens, J. (2019). An aggregon in conductin/axin2 regulates Wnt/β-catenin signaling and holds potential for cancer therapy. Nature communications, 10(1), 1-14.

Chen, M., Liu, Y. Y., Zheng, M. Q., Wang, X. L., Gao, X. H., Chen, L., & Zhang, G. M. (2018). microRNA-544 promoted human osteosarcoma cell proliferation by downregulating AXIN2 expression. Oncology letters, 15(5), 7076-7082.

Haddaji Mastouri, M., De Coster, P., Zaghabani, A., Jammali, F., Raouahi, N., Ben Salem, A., ... & H'mida Ben Brahim, D. (2018). Genetic study of non‐syndromic tooth agenesis through the screening of paired box 9, msh homeobox 1, axin 2, and Wnt family member 10A genes: a case‐series. European journal of oral sciences, 126(1), 24-32.

Hloušková, A., Bielik, P., Bonczek, O., Balcar, V. J., & Šerý, O. (2017). Mutations in AXIN2 gene as a risk factor for tooth agenesis and cancer: A review. Neuroendocrinology Letters, 38(3).

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For research use only. Not intended for any clinical use.

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