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Rabbit Anti-MEN1 Recombinant Antibody (D45B1) (CBMAB-CP1502-LY)

The product is antibody recognizes Menin. The antibody D45B1 immunoassay techniques such as: WB,IF (ICC).
See all MEN1 antibodies

Summary

Host Animal
Rabbit
Specificity
Human, Mouse, Rat, Monkey, Cattle, Pig, Horse
Clone
D45B1
Antibody Isotype
IgG
Application
WB, IF (ICC)

Basic Information

Immunogen
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val597 of human Menin protein.
Specificity
Human, Mouse, Rat, Monkey, Cattle, Pig, Horse
Antibody Isotype
IgG
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
Buffer
100 µg/ml BSA, 50% glycerol
Preservative
0.02% sodium azide
Purity
> 95% Purity determined by SDS-PAGE.
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
MEN1
Entrez Gene ID
Human4221
Mouse17283
Rat29417
Cattle539431
Monkey106995582
Pig100523533
Horse100050500
UniProt ID
HumanO00255
MouseO88559
RatQ9WVR8
CattleQ0P5I0
MonkeyH9FUK1
PigF1RQR2
HorseF6TJ70
Function
Essential component of a MLL/SET1 histone methyltransferase (HMT) complex, a complex that specifically methylates 'Lys-4' of histone H3 (H3K4). Functions as a transcriptional regulator. Binds to the TERT promoter and represses telomerase expression. Plays a role in TGFB1-mediated inhibition of cell-proliferation, possibly regulating SMAD3 transcriptional activity. Represses JUND-mediated transcriptional activation on AP1 sites, as well as that mediated by NFKB subunit RELA. Positively regulates HOXC8 and HOXC6 gene expression. May be involved in normal hematopoiesis through the activation of HOXA9 expression (By similarity).

May be involved in DNA repair.
Biological Process
Brain development Source: Ensembl
Cellular response to DNA damage stimulus Source: UniProtKB
Cellular response to glucose stimulus Source: Ensembl
Cellular response to peptide hormone stimulus Source: Ensembl
Chromatin organization Source: UniProtKB-KW
Decidualization Source: Ensembl
DNA repair Source: UniProtKB
Histone H3-K4 methylation Source: UniProtKB
MAPK cascade Source: UniProtKB
Mitotic cell cycle Source: Ensembl
Negative regulation of cell cycle Source: UniProtKB
Negative regulation of cell cycle G1/S phase transition Source: Ensembl
Negative regulation of cell population proliferation Source: UniProtKB
Negative regulation of cell-substrate adhesion Source: Ensembl
Negative regulation of cyclin-dependent protein serine/threonine kinase activity Source: UniProtKB
Negative regulation of DNA-binding transcription factor activity Source: UniProtKB
Negative regulation of epithelial cell proliferation Source: Ensembl
Negative regulation of JNK cascade Source: UniProtKB
Negative regulation of osteoblast differentiation Source: MGI
Negative regulation of protein phosphorylation Source: UniProtKB
Negative regulation of telomerase activity Source: UniProtKB
Negative regulation of transcription, DNA-templated Source: UniProtKB
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Osteoblast development Source: MGI
Positive regulation of protein binding Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: UniProtKB
Positive regulation of transforming growth factor beta receptor signaling pathway Source: UniProtKB
Regulation of activin receptor signaling pathway Source: Ensembl
Regulation of transcription by RNA polymerase II Source: GO_Central
Regulation of type B pancreatic cell proliferation Source: Ensembl
Response to gamma radiation Source: UniProtKB
Response to transforming growth factor beta Source: Ensembl
Response to UV Source: UniProtKB
Type B pancreatic cell differentiation Source: Ensembl
Cellular Location
Nucleus
Note: Concentrated in nuclear body-like structures. Relocates to the nuclear matrix upon gamma irradiation.
Involvement in disease
Familial multiple endocrine neoplasia type I (MEN1):
Autosomal dominant disorder characterized by tumors of the parathyroid glands, gastro-intestinal endocrine tissue, the anterior pituitary and other tissues. Cutaneous lesions and nervous-tissue tumors can exist. Prognosis in MEN1 patients is related to hormonal hypersecretion by tumors, such as hypergastrinemia causing severe peptic ulcer disease (Zollinger-Ellison syndrome, ZES), primary hyperparathyroidism, and acute forms of hyperinsulinemia.
MEN1 inactivating mutations are responsible for hyperfunctioning of the parathyroid glands and subsequent primary hyperparathyroidism. Primary hyperparathyroidism can occur in isolation or in association with multiple endocrine neoplasia.

Perner, F., Stein, E. M., Wenge, D. V., Singh, S., Kim, J., Apazidis, A., ... & Cai, S. F. (2023). MEN1 mutations mediate clinical resistance to menin inhibition. Nature, 615(7954), 913-919.

Duan, S., Sheriff, S., Elvis-Offiah, U. B., Witten, B. L., Sawyer, T. W., Sundaresan, S., ... & Merchant, J. L. (2023). Clinically defined mutations in MEN1 alter its tumor-suppressive function through increased menin turnover. Cancer Research Communications, 3(7), 1318-1334.

Dreijerink, K. M., Ozyerli-Goknar, E., Koidl, S., van der Lelij, E. J., van den Heuvel, P., Kooijman, J. J., ... & Timmers, H. M. (2022). Multi-omics analyses of MEN1 missense mutations identify disruption of menin–MLL and menin–JunD interactions as critical requirements for molecular pathogenicity. Epigenetics & chromatin, 15(1), 29.

Welsch, C., Flügel, A. K., Rondot, S., Schulze, E., Sircar, I., Nußbaumer, J., & Bojunga, J. (2022). Distinct clinical phenotypes in a family with a novel truncating MEN1 frameshift mutation. BMC Endocrine Disorders, 22(1), 1-8.

Kooblall, K. G., Boon, H., Cranston, T., Stevenson, M., Pagnamenta, A. T., Rogers, A., ... & Thakker, R. V. (2021). Multiple endocrine neoplasia type 1 (MEN1) 5′ UTR deletion, in MEN1 family, decreases Menin expression. Journal of Bone and Mineral Research, 36(1), 100-109.

Qiu, H., Jin, B. M., Wang, Z. F., Xu, B., Zheng, Q. F., Zhang, L., ... & Jin, G. H. (2020). MEN1 deficiency leads to neuroendocrine differentiation of lung cancer and disrupts the DNA damage response. Nature Communications, 11(1), 1009.

Kamilaris, C. D., & Stratakis, C. A. (2019). Multiple endocrine neoplasia type 1 (MEN1): an update and the significance of early genetic and clinical diagnosis. Frontiers in endocrinology, 10, 339.

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

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We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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