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Mouse Anti-MITF Recombinant Antibody (A1098) (CBMAB-AP4468LY)

The product is antibody recognizes MITF. The antibody A1098 immunoassay techniques such as: FC, IF, IHC.
See all MITF antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
A1098
Antibody Isotype
IgG1, κ
Application
FC, IF, IHC

Basic Information

Immunogen
NH2 terminus fragment of human Mi protein
Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Purity
Affinity purity
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Melanogenesis Associated Transcription Factor
Introduction
The protein encoded by this gene is a transcription factor that contains both basic helix-loop-helix and leucine zipper structural features. The encoded protein regulates melanocyte development and is responsible for pigment cell-specific transcription of the melanogenesis enzyme genes. Heterozygous mutations in the this gene cause auditory-pigmentary syndromes, such as Waardenburg syndrome type 2 and Tietz syndrome. [provided by RefSeq, Aug 2017]
Entrez Gene ID
4286
UniProt ID
O75030
Alternative Names
Melanogenesis Associated Transcription Factor; Microphthalmia-Associated Transcription Factor; Class E Basic Helix-Loop-Helix Protein 32; BHLHe32; Microphtalmia-Associated Transcription Factor; Homolog Of Mouse Microphthalmia; Waardenburg Syndrome, Type 2A;
Function
Transcription factor that regulates the expression of genes with essential roles in cell differentiation, proliferation and survival. Binds to M-boxes (5'-TCATGTG-3') and symmetrical DNA sequences (E-boxes) (5'-CACGTG-3') found in the promoters of target genes, such as BCL2 and tyrosinase (TYR). Plays an important role in melanocyte development by regulating the expression of tyrosinase (TYR) and tyrosinase-related protein 1 (TYRP1). Plays a critical role in the differentiation of various cell types, such as neural crest-derived melanocytes, mast cells, osteoclasts and optic cup-derived retinal pigment epithelium.
Biological Process
Bone remodeling Source: Ensembl
Camera-type eye development Source: Ensembl
Canonical Wnt signaling pathway involved in negative regulation of apoptotic process Source: Ensembl
Cell fate commitment Source: Ensembl
Melanocyte differentiation Source: GO_Central
Negative regulation of cell migration Source: BHF-UCL
Negative regulation of transcription by RNA polymerase II Source: BHF-UCL
Osteoclast differentiation Source: Ensembl
Positive regulation of DNA-templated transcription, initiation Source: CACAO
Positive regulation of gene expression Source: CACAO
Positive regulation of transcription, DNA-templated Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: UniProtKB
Protein-containing complex assembly Source: UniProtKB
Regulation of cell population proliferation Source: Ensembl
Regulation of osteoclast differentiation Source: Ensembl
Regulation of RNA biosynthetic process Source: CACAO
Regulation of transcription, DNA-templated Source: UniProtKB
Regulation of transcription by RNA polymerase II Source: GO_Central
Cellular Location
Cytoplasm 1 Publication
Nucleus
Note: Found exclusively in the nucleus upon phosphorylation.
Involvement in disease
Waardenburg syndrome 2A (WS2A):
WS2 is a genetically heterogeneous, autosomal dominant disorder characterized by sensorineural deafness, pigmentary disturbances, and absence of dystopia canthorum. The frequency of deafness is higher in WS2 than in WS1.
Tietz albinism-deafness syndrome (TADS):
An autosomal dominant disorder characterized by generalized hypopigmentation and congenital, bilateral, profound sensorineural deafness.
Melanoma, cutaneous malignant 8 (CMM8):
A malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.
Coloboma, osteopetrosis, microphthalmia, macrocephaly, albinism, and deafness (COMMAD):
An autosomal recessive syndrome characterized by severe microphthalmia, profound congenital sensorineural hearing loss, lack of pigment in the hair, skin, and eyes, macrocephaly, facial dysmorphism, and osteopetrosis.
PTM
Phosphorylation at Ser-405 significantly enhances the ability to bind the tyrosinase promoter (PubMed:10587587). Phosphorylated at Ser-180 and Ser-516 following KIT signaling, triggering a short live activation: Phosphorylation at Ser-180 and Ser-516 by MAPK and RPS6KA1, respectively, activate the transcription factor activity but also promote ubiquitination and subsequent degradation by the proteasome (PubMed:10673502). Phosphorylated in response to blue light (415nm) (PubMed:28842328).
Ubiquitinated following phosphorylation at Ser-180, leading to subsequent degradation by the proteasome. Deubiquitinated by USP13, preventing its degradation.

Gelmi, M. C., Houtzagers, L. E., Strub, T., Krossa, I., & Jager, M. J. (2022). Mitf in normal melanocytes, cutaneous and uveal melanoma: a delicate balance. International journal of molecular sciences, 23(11), 6001.

Truong, X. T., Lee, Y. S., Nguyen, T. T., Kim, H. J., Kim, S. H., Moon, C., ... & Jeon, T. I. (2022). SMILE Downregulation during Melanogenesis Induces MITF Transcription in B16F10 Cells. International Journal of Molecular Sciences, 23(23), 15094.

Abrahamian, C., & Grimm, C. (2021). Endolysosomal cation channels and MITF in melanocytes and melanoma. Biomolecules, 11(7), 1021.

Yun, C. Y., Roh, E., Kim, S. H., Han, J., Lee, J., Jung, D. E., ... & Kim, Y. (2020). Stem cell factor-inducible MITF-M expression in therapeutics for acquired skin hyperpigmentation. Theranostics, 10(1), 340.

Lv, J., Fu, Y., Cao, Y., Jiang, S., Yang, Y., Song, G., ... & Gao, R. (2020). Isoliquiritigenin inhibits melanogenesis, melanocyte dendricity and melanosome transport by regulating ERK‐mediated MITF degradation. Experimental Dermatology, 29(2), 149-157.

Kim, J. H., Hong, A. R., Kim, Y. H., Yoo, H., Kang, S. W., Chang, S. E., & Song, Y. (2020). JNK suppresses melanogenesis by interfering with CREB-regulated transcription coactivator 3-dependent MITF expression. Theranostics, 10(9), 4017.

Flesher, J. L., Paterson‐Coleman, E. K., Vasudeva, P., Ruiz‐Vega, R., Marshall, M., Pearlman, E., ... & Ganesan, A. K. (2020). Delineating the role of MITF isoforms in pigmentation and tissue homeostasis. Pigment cell & melanoma research, 33(2), 279-292.

Raja, D. A., Gotherwal, V., Burse, S. A., Subramaniam, Y. J., Sultan, F., Vats, A., ... & Natarajan, V. T. (2020). pH‐controlled histone acetylation amplifies melanocyte differentiation downstream of MITF. EMBO reports, 21(1), e48333.

Basu, R., Kulkarni, P., Qian, Y., Walsh, C., Arora, P., Davis, E., ... & Kopchick, J. J. (2019). Growth hormone upregulates melanocyte-inducing transcription factor expression and activity via JAK2-STAT5 and SRC signaling in GH receptor-positive human melanoma. Cancers, 11(9), 1352.

Goding, C. R., & Arnheiter, H. (2019). MITF—the first 25 years. Genes & development, 33(15-16), 983-1007.

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For research use only. Not intended for any clinical use.

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