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MiTF Mouse mAb

Catalog No.: F1169

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000

Application
WB, IF, FCM

Reactivity
Human

Source
Mouse

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
59 kDa 40 kDa,55 kDa,70 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Datasheet & SDS

Biological Description

Specificity
MiTF Mouse mAb detects endogenous levels of total MiTF protein.

Clone
M6F11

Synonym(s)
BHLHE32, MITF, Microphthalmia-associated transcription factor, Class E basic helix-loop-helix protein 32, bHLHe32

Background
The microphthalmia-associated transcription factor (MITF) is a key regulator involved in the differentiation and development of melanocytes and retinal pigment epithelium (RPE). It is also essential for pigment cell-specific transcription of genes encoding melanogenesis enzymes. Heterozygous mutations in the MITF gene are linked to auditory–pigmentary syndromes. MITF exists in at least five isoforms—MITF-A, MITF-B, MITF-C, MITF-H, and MITF-M—which differ at their N-terminal regions and exhibit distinct expression patterns. In mice, the Mitf gene plays a critical role in the development and/or survival of various cell lineages, including melanocytes, RPE, mast cells, and osteoclasts. Both mouse Mitf and human MITF proteins possess a basic helix–loop–helix–leucine zipper (bHLH-LZ) domain, enabling DNA binding and dimerization. All isoforms with extended N-terminal sequences share the same C-terminal portion as MITF-M. MITF-A is the predominant isoform in a fetal-derived human RPE cell line and is also present in multiple other cell types. Its N-terminal “Domain A” shares significant amino acid similarity with the N-terminus of TFE3. MITF serves as a master regulator of melanocyte-specific genes and is indispensable for proper melanocyte lineage development. Dysregulation of MITF activity can contribute to disease pathogenesis, notably melanoma, in which MITF functions as an amplified oncogene. For transcriptional activation, MITF recruits the co-activators CREB-binding protein (CBP) and its homolog p300 to gene promoters. The transcriptional potential of its C-terminal region depends on the N-terminal transactivation domain for full functionality.

Background

The microphthalmia-associated transcription factor (MITF) is a key regulator involved in the differentiation and development of melanocytes and retinal pigment epithelium (RPE). It is also essential for pigment cell-specific transcription of genes encoding melanogenesis enzymes. Heterozygous mutations in the MITF gene are linked to auditory–pigmentary syndromes. MITF exists in at least five isoforms—MITF-A, MITF-B, MITF-C, MITF-H, and MITF-M—which differ at their N-terminal regions and exhibit distinct expression patterns. In mice, the Mitf gene plays a critical role in the development and/or survival of various cell lineages, including melanocytes, RPE, mast cells, and osteoclasts. Both mouse Mitf and human MITF proteins possess a basic helix–loop–helix–leucine zipper (bHLH-LZ) domain, enabling DNA binding and dimerization. All isoforms with extended N-terminal sequences share the same C-terminal portion as MITF-M. MITF-A is the predominant isoform in a fetal-derived human RPE cell line and is also present in multiple other cell types. Its N-terminal “Domain A” shares significant amino acid similarity with the N-terminus of TFE3. MITF serves as a master regulator of melanocyte-specific genes and is indispensable for proper melanocyte lineage development. Dysregulation of MITF activity can contribute to disease pathogenesis, notably melanoma, in which MITF functions as an amplified oncogene. For transcriptional activation, MITF recruits the co-activators CREB-binding protein (CBP) and its homolog p300 to gene promoters. The transcriptional potential of its C-terminal region depends on the N-terminal transactivation domain for full functionality.

References
https://pubmed.ncbi.nlm.nih.gov/11764295/ https://www.nature.com/articles/s41598-023-43207-6

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%