Mouse Homeobox protein aristaless-like 4 (ALX4) ELISA kit; KIAA1788; aristaless-like homeobox 4; homeodomain transcription factor ALX4; ALX homeobox 4

For Research Use Only. Not for use in diagnostic procedures.

Store all reagents at 2-8 degree C

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Small volumes of ALX4 elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS9318912 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the ALX homeobox 4 (ALX4) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing ALX4. The ELISA analytical biochemical technique of the MBS9318912 kit is based on ALX4 antibody-ALX4 antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect ALX4 antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, ALX4. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

42,763 Da

aristaless-like homeobox 4

homeobox protein aristaless-like 4; ALX-4; aristaless 4; Strong's luxoid; Aristaless-like 4

Homeobox protein aristaless-like 4

ALX4_MOUSE

ALX4: Transcription factor involved in skull and limb development. Plays an essential role in craniofacial development, skin and hair follicle development. Defects in ALX4 are the cause of parietal foramina 2 (P***); also known as foramina parietalia permagna (FPP). P*** is an 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. P*** is also a clinical feature of Potocki- Shaffer syndrome. Defects in ALX4 are the cause of frontonasal dysplasia type 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. Defects in ALX4 are a cause of Potocki-Shaffer syndrome (POSHS). A contiguous gene syndrome caused by deletion of the 11p11.2 region. Belongs to the paired homeobox family.

Protein type: DNA-binding

Cellular Component: transcription factor complex; nucleus

Molecular Function: protein binding; DNA binding; sequence-specific DNA binding; protein heterodimerization activity; transcription factor activity

Biological Process: embryonic forelimb morphogenesis; transcription from RNA polymerase II promoter; muscle development; transcription, DNA-dependent; multicellular organismal development; palate development; pattern specification process; limb morphogenesis; embryonic hindlimb morphogenesis; embryonic skeletal morphogenesis; post-embryonic development; regulation of transcription from RNA polymerase II promoter; regulation of apoptosis; anterior/posterior pattern formation; regulation of transcription, DNA-dependent; hair follicle development; gut development; skeletal morphogenesis; positive regulation of transcription from RNA polymerase II promoter; embryonic digit morphogenesis

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