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Mouse Anti-ALX4 Recombinant Antibody (KAbB4) (CBMAB-AP297LY)


See all ALX4 antibodies
Published Data
Mouse Anti-ALX4 Recombinant Antibody (KAbB4) in IHC
Immunohistochemical staining for VCAN and ALX4 (arrow heads) around outgrowing ductal epithelium in 3-days pregnant mouse mammary glands and in glands from age-matched adult virgin glands (representative images, n = 4 (VCAN) and 3 (ALX4) animals respectively; see also Additional file 6: Figure S4). Scale bars are 100 µm. ...View More
Ibrahim, A. M., Bilsland, A., Rickelt, S., Morris, J. S., & Stein, T. (2021). A matrisome RNA signature from early-pregnancy mouse mammary fibroblasts predicts distant metastasis-free breast cancer survival in humans. Breast Cancer Research, 23(1), 1-19.
Mouse Anti-ALX4 Recombinant Antibody (KAbB4) in WB
Western blot were used to detect the effects of circ_0000098 and miR-1204 on ALX4 expression in Huh7 and SMMC-7721 cells. ...View More
Li, M., Yue, W., Li, Q., Yu, W., Li, Y., & Cao, X. (2021). Circular RNA Circ_0000098 elevates ALX4 expression via adsorbing miR-1204 to inhibit the progression of hepatocellular carcinoma. Frontiers in Oncology, 11, 696078.
Mouse Anti-ALX4 Recombinant Antibody (KAbB4) in IHC
In new born pups, Alx1, Alx4 and Fgf10 were expressed in the lacrimal gland mesenchyme, whereas the FGF response gene Etv5 was expressed in the epithelium. ...View More
Garg, A., Bansal, M., Gotoh, N., Feng, G. S., Zhong, J., Wang, F., ... & Zhang, X. (2017). Alx4 relays sequential FGF signaling to induce lacrimal gland morphogenesis. PLoS Genetics, 13(10), e1007047.

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
KAbB4
Antibody Isotype
IgG1, κ
Application
ELISA, IHC-P, IP, WB, IF

Basic Information

Immunogen
Recombinant full length ALX4 of mouse origin.
Host Species
Mouse
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
ELISA1:30-1:3,000
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
IHC1:50-1:500

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

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
ALX Homeobox 4
Introduction
This gene encodes a paired-like homeodomain transcription factor expressed in the mesenchyme of developing bones, limbs, hair, teeth, and mammary tissue. Mutations in this gene cause parietal foramina 2 (PFM2); an autosomal dominant disease characterized by deficient ossification of the parietal bones. Mutations in this gene also cause a form of frontonasal dysplasia with alopecia and hypogonadism; suggesting a role for this gene in craniofacial development, mesenchymal-epithelial communication, and hair follicle development. Deletion of a segment of chromosome 11 containing this gene, del(11)(p11p12), causes Potocki-Shaffer syndrome (PSS); a syndrome characterized by craniofacial anomalies, cognitive disability, multiple exostoses, and genital abnormalities in males. In mouse, this gene has been shown to use dual translation initiation sites located 16 codons apart. [provided by RefSeq, Oct 2009]
Entrez Gene ID
11695
UniProt ID
O35137
Alternative Names
ALX Homeobox 4; Aristaless-Like Homeobox 4; Homeodomain Transcription Factor ALX4; Homeobox Protein Aristaless-Like 4; Parietal Foramina 2; KIAA1788; CRS5; FND2;
Function
Transcription factor involved in skull and limb development. Plays an essential role in craniofacial development, skin and hair follicle development.
Biological Process
Anterior/posterior pattern specification Source: Ensembl
Digestive tract development Source: Ensembl
Embryonic digit morphogenesis Source: Ensembl
Embryonic forelimb morphogenesis Source: Ensembl
Embryonic hindlimb morphogenesis Source: Ensembl
Embryonic skeletal system morphogenesis Source: Ensembl
Hair follicle development Source: UniProtKB
Muscle organ development Source: Ensembl
Post-embryonic development Source: Ensembl
Regulation of apoptotic process Source: Ensembl
Regulation of transcription by RNA polymerase II Source: GO_Central
Roof of mouth development Source: Ensembl
Skeletal system development Source: UniProtKB
Cellular Location
Nucleus
Involvement in disease
Parietal foramina 2 (PFM2): Autosomal dominant disease characterized by oval defects of the parietal bones caused by deficient ossification around the parietal notch, which is normally obliterated during the fifth fetal month. PFM2 is also a clinical feature of Potocki-Shaffer syndrome.
Frontonasal dysplasia 2 (FND2): The term frontonasal dysplasia describes an array of abnormalities affecting the eyes, forehead and nose and linked to midfacial dysraphia. The clinical picture is highly variable. Major findings include true ocular hypertelorism; broadening of the nasal root; median facial cleft affecting the nose and/or upper lip and palate; unilateral or bilateral clefting of the alae nasi; lack of formation of the nasal tip; anterior cranium bifidum occultum; a V-shaped or widow's peak frontal hairline.
Potocki-Shaffer syndrome (POSHS): A syndrome characterized by foramina parietalia permagna, multiple exostoses, and craniofacial dysostosis and mental retardation in some cases.
Craniosynostosis 5 (CRS5): A primary abnormality of skull growth involving premature fusion of one or more cranial sutures. The growth velocity of the skull often cannot match that of the developing brain resulting in an abnormal head shape and, in some cases, increased intracranial pressure, which must be treated promptly to avoid permanent neurodevelopmental disability.
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For research use only. Not intended for any clinical use.

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We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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