Oncogene Research Products, Calbiochem, Novagen, Merck, Upstate Biotechnology, Chemicon, LINCO, Novabiochem, Guava

antibody

Microphthalmia (Mi) Antibody, clone C5

MAB3747-I

100 μg

monoclonal

mouse

nonconjugated

C5

The same clone is also sold as:

• OriGene: AM05308PU-N
• Abnova: MAB1955
• Abcam: ab12039
• Exalpha Biologicals: X1405M
• Santa Cruz Biotechnology: sc-56725
• MilliporeSigma: M6065
• Novus Biologicals: NB110-10872

human, mouse

western blot, immunohistochemistry

Epigenetics & Nuclear Function

Anti-Microphthalmia (Mi) Antibody, clone C5

Antibodies

Monoclonal Antibody

O75030

Mouse

Microphthalmia (Mi)

C5

Purified

IgG2aκ;IgG 1 κ

Anti-Microphthalmia (Mi) Antibody, clone C5

Human;Mouse

MiTF (Microphthalmia associated transcription factor) is a basic helix loop helix leucine zipper (b HLH ZIP) transcription factor implicated in pigmentation, mast cells and bone development. Mutations in MiTF cause auditory pigmentary syndromes, such as Waardenburg syndrome type II, type IIa and Tietz syndrome in humans. There are two known isoforms of MiTF differing by 66 amino acids at the NH2 terminus. Shorter forms are expressed in melanocytes and run as two bands at 52 kDa and 56 kDa, while the longer Mi form runs as a cluster of bands at 60-70 kDa in osteoclasts and in B16 melonoma cells (but not other melanoma cell lines), as well as mast cells and heart. MiTF plays a critical role in the differentiation of various cell types as neural crest-derived melanocytes, mast cells, osteoclasts and optic cup-derived retinal pigment epithelium. Mi is a basic helix-loop-helix-leucine zipper (b-HLH-ZIP) transcription factor implicated in pigmentation, mast cells and bone development. The mutation of Mi causes Waardenburg Syndrome type II in humans. In mice, a profound loss of pigmented cells in the skin eye and inner ear results, as well as osteopetrosis and defects in natural killer and mast cells. These melanocyte isoforms have been shown by two dimensional tryptic mapping to differ in c-Kit-induced phosphorylation. Osteopetrotic rat strain harbors a large genomic deletion encompassing the 3' half of Mi including most of the b-HLH-ZIP region. Osteoclasts from these animals lack Mi protein in contrast to wild-type rat, mouse, and human osteoclasts.

Microphthalmia-associated transcription factor;Class E basic helix-loop-helix protein 32;bHLHe32

Hybridoma produced by the fusion of splenocytes from RBF/DnJ mice immunized with an N-terminal fragment of human microphthalmia protein and mouse myeloma NS1 cells.

In Western blotting, it recognizes a doublet of 52-56 kDa, identified as serine-phosphorylated and unphosphorylated forms of melanocytic isoforms of microphthalmia (Mi). There are two known isoforms of Mi differing by 66 amino acids at the NH2 terminus. Shorter forms are expressed in melanocytes and run as two bands at 52 kDa and 56 kDa, while the longer Mi form runs as a cluster of bands at 60-70 kDa in osteoclasts and in B16 melonoma cells (but not other melanoma cell lines), as well as mast cells andheart. It reacts with both melanocytic as well as the nonmelanocytic isoforms of Mi. This Ab does not cross-react with other b-HLH-ZIP factors by DNA mobility shift assay.

100 μg

Western Blotting;Immunohistochemistry

Stable for 1 year at 2-8°C from date of receipt