MAB3747
Anti-Microphthalmia (Mi) Antibody, clone C5
clone C5, Chemicon®, from mouse
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
C5, monoclonal
species reactivity
mouse
species reactivity (predicted by homology)
human, rat
manufacturer/tradename
Chemicon®
technique(s)
electrophoretic mobility shift assay: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
immunoprecipitation (IP): suitable
western blot: suitable
isotype
IgG1
shipped in
wet ice
target post-translational modification
unmodified
General description
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-leucin zipper (b-HLH-ZIP) transtripotion 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.
Specificity
In Western blotting, it recognizes a doublet of 52-56kDa, 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 52kDa and 56kDa, while the longer Mi form runs as a cluster of bands at 60-70kDa 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.
Immunogen
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.
Application
Anti-Microphthalmia (Mi) Antibody, clone C5 is a Mouse Monoclonal Antibody for detection of Microphthalmia (Mi) also known as Microphthalmia-associated transcription factor & has been tested in EMSA, IHC, IHC(P), IP & WB.
Immunoprecipitation:
A previous lot of this antibody was used in IP. (2 µg/mg of protein lysate)
Gel supershift assays:
A previous lot of this antibody was used in EMSA.
Immunohistochemistry(paraffin):
A previous lot of this antibody was used in IH on frozen and formalin/paraffin tissue sections.
Optimal working dilutions must be determined by end user.
A previous lot of this antibody was used in IP. (2 µg/mg of protein lysate)
Gel supershift assays:
A previous lot of this antibody was used in EMSA.
Immunohistochemistry(paraffin):
A previous lot of this antibody was used in IH on frozen and formalin/paraffin tissue sections.
Optimal working dilutions must be determined by end user.
Quality
Routinely evaluated by Western Blot on Mouse Brain lysates.
Western Blot Analysis:
1:500 dilution of this lot detected Mi on 10 μg of Mouse Brain lysates.
Western Blot Analysis:
1:500 dilution of this lot detected Mi on 10 μg of Mouse Brain lysates.
Target description
53-56 kDa
Physical form
Format: Purified
Purified mouse monoclonal IgG1 in phosphate buffered saline with 0.08% sodium azide.
Storage and Stability
Stable for 1 year at -20ºC in undiluted aliquots from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage the IgG1 and affect product performance.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage the IgG1 and affect product performance.
Analysis Note
Control
501 Mel human melanoma cells, wild-type human, rat, mouse osteoclast cells.
501 Mel human melanoma cells, wild-type human, rat, mouse osteoclast cells.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Find documentation for the products that you have recently purchased in the Document Library.
Pakavarin Louphrasitthiphol et al.
Molecular cell, 79(3), 472-487 (2020-06-13)
It is widely assumed that decreasing transcription factor DNA-binding affinity reduces transcription initiation by diminishing occupancy of sequence-specific regulatory elements. However, in vivo transcription factors find their binding sites while confronted with a large excess of low-affinity degenerate motifs. Here, using
Anai Gonzalez-Cordero et al.
Human gene therapy, 29(10), 1124-1139 (2018-03-28)
Adeno-associated viral vectors are showing great promise as gene therapy vectors for a wide range of retinal disorders. To date, evaluation of therapeutic approaches has depended almost exclusively on the use of animal models. With recent advances in human stem
Luis Sánchez-Del-Campo et al.
Journal of experimental & clinical cancer research : CR, 40(1), 117-117 (2021-04-02)
The application of immune-based therapies has revolutionized cancer treatment. Yet how the immune system responds to phenotypically heterogeneous populations within tumors is poorly understood. In melanoma, one of the major determinants of phenotypic identity is the lineage survival oncogene MITF
Chelsey D Kline et al.
Cancers, 14(20) (2022-10-28)
TR1 and other selenoproteins have paradoxical effects in melanocytes and melanomas. Increasing selenoprotein activity with supplemental selenium in a mouse model of UV-induced melanoma prevents oxidative damage to melanocytes and delays melanoma tumor formation. However, TR1 itself is positively associated
Marcos Seoane et al.
Oncogene, 38(19), 3616-3635 (2019-01-18)
The melanocytic lineage, which is prominently exposed to ultraviolet radiation (UVR) and radiation-independent oxidative damage, requires specific DNA-damage response mechanisms to maintain genomic and transcriptional homeostasis. The coordinate lineage-specific regulation of intricately intertwined DNA repair and transcription is incompletely understood.
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