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Use Anti-Microphthalmia (Mi), clone C5 mouse monoclonal antibody validated in Electrophoretic Mobility Shift Assay (EMSA), Immunocytochemistry, Immunohistochemistry, Immunoprecipitation and Western blotting for the detection of Microphthalmia-associated transcription factor.
More>>Use Anti-Microphthalmia (Mi), clone C5 mouse monoclonal antibody validated in Electrophoretic Mobility Shift Assay (EMSA), Immunocytochemistry, Immunohistochemistry, Immunoprecipitation and Western blotting for the detection of Microphthalmia-associated transcription factor. Less<<
Anti-Microphthalmia (Mi) Antibody, clone C5: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
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.
References
Product Information
Format
Purified
Control
Mouse brain tissue lysates
Presentation
Purified mouse monoclonal IgG2aκ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Use Anti-Microphthalmia (Mi), clone C5 mouse monoclonal antibody validated in Electrophoretic Mobility Shift Assay (EMSA), Immunocytochemistry, Immunohistochemistry, Immunoprecipitation and Western blotting for the detection of Microphthalmia-associated transcription factor.
Key Applications
Western Blotting
Immunohistochemistry
Immunofluorescence
Immunocytochemistry
Electrophoretic Mobility Shift Assay
Immunoprecipitation
Application Notes
Immunohistochemistry Analysis: A representative lot detected microphthalmia immunoreactivity in formalin-fixed, paraffin-embedded human metastatic melanoma tissue sections by fluorescent immunohistochemistry (Feige, E., et. al. (2011). Proc. Natl .Acad. Sci. U. S. A. 108(43):E924-E933). Immunocytochemistry Analysis: A representative lot detected the exogenously expressed murine microphthalmia mutant constructs, Mitf D222/236N and Mitf D222N (mi-vit), in the nucleus of transfected COS-7 cells. Dual staining showed much reduced β-catenin-anchoring ability of these mutants in the nucleus (Schepsky, A., et al. (2006). Mol. Cell. Biol. 26(23): 8914-8927). Immunocytochemistry Analysis: A representative lot detected a time-dependent induction of microphthalmia upregulation in B16/F10 murine melanoma cells upon Forskolin stimulation by fluorescent immunocytochemistry (Bertolotto, C., et al. (1998). J. Cell Biol. 142(3):827-835). Electrophoretic Mobility Shift Assay (EMSA): A representative lot caused a supershift of Mbox motif oligonucleotide-complexed wild-type and D222/236N and D222N mutant murine microphthalmia constructs by EMSA (Schepsky, A., et al. (2006). Mol. Cell. Biol. 26(23): 8914-8927). Electrophoretic Mobility Shift Assay (EMSA): A representative lot caused a supershift of Mbox motif oligonucleotide-complexed microphthalmia, but not TFE3-DNA complex by EMSA using in vitro translated microphthalmia and TFE3 or B16/F10 murine melanoma cell nuclear extract (Verastegui, C., et al. (2000). Mol. Endocrinol. 14(3):449-456). Immunoprecipitation Analysis: A representative lot immunoprecipitated microphthalmia from B16/F10 murine melanoma cell nuclear extracts (Verastegui, C., et al. (2000). Mol. Endocrinol. 14(3):449-456). Western Blotting Analysis: A representative lot detected microphthalmia expression in murine splenocytes and B16/F10 murine melanoma cells (Verastegui, C., et al. (2000). Mol. Endocrinol. 14(3):449-456). Western Blotting Analysis: A representative lot detected a time-dependent induction of microphthalmia upregulation in B16/F10 murine melanoma cells and normal human melanocytes upon stimulation by Forskolin or α-melanocyte–stimulating hormone (αMSH) (Bertolotto, C., et al. (1998). J. Cell Biol. 142(3):827-835).
Biological Information
Immunogen
Recombinant N-terminal fragment of human microphthalmia protein.
Epitope
N-terminal
Clone
C5
Concentration
Please refer to the Certificate of Analysis for the lot-specific concentration.
Host
Mouse
Specificity
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.
Isotype
IgG1κ
Species Reactivity
Human
Mouse
Species Reactivity Note
Human and Mouse. Predicted to react with Rat based on sequence homology.
~52/56 kDa observed. An uncharacterized band appears at ~140 kDa in some lysates.
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blotting in mouse brain tissue lysate.
Western Blotting Analysis: An 1:500 dilution of this antibody detected Microphthalmia in 10 µg of mouse brain tissue lysate.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Melanogenesis-inducing effect of cirsimaritin through increases in microphthalmia-associated transcription factor and tyrosinase expression. Kim, HJ; Kim, IS; Dong, Y; Lee, IS; Kim, JS; Kim, JS; Woo, JT; Cha, BY International journal of molecular sciences
16
8772-88
2015
The melanin-inducing properties of cirsimaritin were investigated in murine B16F10 cells. Cirsimaritin is an active flavone with methoxy groups, which is isolated from the branches of Lithocarpus dealbatus. Tyrosinase activity and melanin content in murine B16F10 melanoma cells were increased by cirsimaritin in a dose-dependent manner. Western blot analysis revealed that tyrosinase, tyrosinase-related protein (TRP) 1, TRP2 protein levels were enhanced after treatment with cirsimaritin for 48 h. Cirsimaritin also upregulated the expression of microphthalmia-associated transcription factor (MITF) after 24 h of treatment. Furthermore, cirsimaritin induced phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) in a dose-dependent manner after treatment for 15 min. The cirsimaritin-mediated increase of tyrosinase activity was significantly attenuated by H89, a cAMP-dependent protein kinase A inhibitor. These findings indicate that cirsimaritin stimulates melanogenesis in B16F10 cells by activation of CREB as well as upregulation of MITF and tyrosinase expression, which was activated by cAMP signaling. Finally, the melanogenic effect of cirsimaritin was confirmed in human epidermal melanocytes. These results support the putative application of cirsimaritin in ultraviolet photoprotection and hair coloration treatments.
Perivascular epithelioid cell neoplasms, also known as PEComas, are unique mesenchymal tumors exhibiting perivascular epithelioid cell differentiation, characterized by a mixed myogenic and melanocytic phenotype. PEComas arising in visceral organs outside of the kidney, liver, and lung are rare, and often pose problems in diagnosis. Examples of this neoplasm originating in the adrenal gland are limited. The present report details the clinical and pathologic features of an unusual case of a pure epithelioid PEComa (epithelioid angiomyolipoma) of the adrenal gland exhibiting clinically malignant behavior in the form of pulmonary metastases, a feature not previously described in tumors of this site. The diagnosis was supported by immunohistochemical studies demonstrating expression of myoid and melanocytic antigens. The present case serves to emphasize the potential of PEComa for clinically aggressive behavior and the importance of distinguishing this tumor from other epithelioid neoplasms that are more commonly encountered in the adrenal gland.
