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Mouse Anti-HNF4A Antibody (2A8) (CBMAB-0493-YC)

Provided herein are mouse monoclonal antibodies against Human HNF4A. The antibody clone 2A8 can be used for immunoassay techniques, such as IP and MA.
See all HNF4A antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
2A8
Antibody Isotype
IgG2a
Application
IP, MA

Basic Information

Immunogen
Recombinant protein
Specificity
Human
Antibody Isotype
IgG2a
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
Supernatant
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Hepatocyte Nuclear Factor 4 Alpha
Introduction
HNF4A (hepatocyte nuclear factor 4, alpha) is a nuclear transcription factor which binds DNA as a homodimer. HNF4A regulates some genes expression, including hepatocyte nuclear factor 1 alpha, a transcription factor which regulates the expression of several hepatic genes. HNF4A may play a role in development of the liver, kidney, and intestines and mutations of it have been associated with monogenic autosomal dominant non-insulin-dependent diabetes mellitus type I.
Entrez Gene ID
3172
UniProt ID
P41235
Alternative Names
TCF; HNF4; MODY; FRTS4; MODY1; NR2A1; TCF14; HNF4a7; HNF4a8; HNF4a9; NR2A21; HNF4alpha
Function
Transcriptional regulator which controls the expression of hepatic genes during the transition of endodermal cells to hepatic progenitor cells, facilitating the recruitment of RNA pol II to the promoters of target genes (PubMed:30597922).

Activates the transcription of CYP2C38 (By similarity).

Represses the CLOCK-ARNTL/BMAL1 transcriptional activity and is essential for circadian rhythm maintenance and period regulation in the liver and colon cells (PubMed:30530698).
Biological Process
Anatomical structure development Source: GO_Central
Blood coagulation Source: BHF-UCL
Cell differentiation Source: GO_Central
Cholesterol homeostasis Source: BHF-UCL
Glucose homeostasis Source: BHF-UCL
Hepatocyte differentiation Source: InterPro
Lipid homeostasis Source: BHF-UCL
Lipid metabolic process Source: Ensembl
Negative regulation of cell growth Source: BHF-UCL
Negative regulation of cell population proliferation Source: BHF-UCL
Negative regulation of transcription, DNA-templated Source: UniProtKB
Ornithine metabolic process Source: BHF-UCL
Phospholipid homeostasis Source: BHF-UCL
Positive regulation of transcription, DNA-templated Source: BHF-UCL
Positive regulation of transcription by RNA polymerase II Source: MGI
Regulation of circadian rhythm Source: UniProtKB
Regulation of gastrulation Source: Ensembl
Regulation of growth hormone receptor signaling pathway Source: BHF-UCL
Regulation of insulin secretion Source: BHF-UCL
Regulation of lipid metabolic process Source: BHF-UCL
Regulation of transcription by RNA polymerase II Source: BHF-UCL
Response to glucose Source: BHF-UCL
Rhythmic process Source: UniProtKB-KW
Sex differentiation Source: Ensembl
Signal transduction involved in regulation of gene expression Source: Ensembl
SMAD protein signal transduction Source: Ensembl
Triglyceride homeostasis Source: BHF-UCL
Type B pancreatic cell development Source: InterPro
Xenobiotic metabolic process Source: BHF-UCL
Cellular Location
Nucleus
Involvement in disease
Maturity-onset diabetes of the young 1 (MODY1):
A form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.
Diabetes mellitus, non-insulin-dependent (NIDDM):
A multifactorial disorder of glucose homeostasis caused by a lack of sensitivity to the body's own insulin. Affected individuals usually have an obese body habitus and manifestations of a metabolic syndrome characterized by diabetes, insulin resistance, hypertension and hypertriglyceridemia. The disease results in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
Fanconi renotubular syndrome 4 with maturity-onset diabetes of the young (FRTS4):
An autosomal dominant disease characterized by Fanconi syndrome associated with a beta cell phenotype of neonatal hyperinsulinism with macrosomia and young onset diabetes. Fanconi syndrome is a proximal tubulopathy resulting in generalized aminoaciduria, low molecular weight proteinuria, glycosuria, hyperphosphaturia and hypouricemia. Some FRTS4 patients have nephrocalcinosis, renal impairment, hypercalciuria with relative hypocalcemia, and hypermagnesemia.
PTM
Phosphorylated on tyrosine residue(s); phosphorylation is important for its DNA-binding activity. Phosphorylation may directly or indirectly play a regulatory role in the subnuclear distribution. Phosphorylation at Ser-313 by AMPK reduces the ability to form homodimers and bind DNA.
Acetylation at Lys-458 lowers transcriptional activation by about two-fold.

Hunter, A. L., Poolman, T. M., Kim, D., Gonzalez, F. J., Bechtold, D. A., Loudon, A. S., ... & Ray, D. W. (2022). HNF4A modulates glucocorticoid action in the liver. Cell Reports, 39(3).

Xu, Y., Zhou, Z., Kang, X., Pan, L., Liu, C., Liang, X., ... & Zhang, Q. (2022). Mettl3-mediated mRNA m6A modification controls postnatal liver development by modulating the transcription factor Hnf4a. Nature Communications, 13(1), 4555.

Yang, T., Poenisch, M., Khanal, R., Hu, Q., Dai, Z., Li, R., ... & Sharma, A. D. (2021). Therapeutic HNF4A mRNA attenuates liver fibrosis in a preclinical model. Journal of Hepatology, 75(6), 1420-1433.

Pan, J., Silva, T. C., Gull, N., Yang, Q., Plummer, J. T., Chen, S., ... & Lin, D. C. (2020). Lineage-specific epigenomic and genomic activation of oncogene HNF4A promotes gastrointestinal adenocarcinomas. Cancer research, 80(13), 2722-2736.

Brunton, H., Caligiuri, G., Cunningham, R., Upstill-Goddard, R., Bailey, U. M., Garner, I. M., ... & Papangelis, V. (2020). HNF4A and GATA6 loss reveals therapeutically actionable subtypes in pancreatic cancer. Cell reports, 31(6).

Marable, S. S., Chung, E., & Park, J. S. (2020). Hnf4a is required for the development of Cdh6-expressing progenitors into proximal tubules in the mouse kidney. Journal of the American Society of Nephrology: JASN, 31(11), 2543.

Marable, S. S., Chung, E., Adam, M., Potter, S. S., & Park, J. S. (2018). Hnf4a deletion in the mouse kidney phenocopies Fanconi renotubular syndrome. JCI insight, 3(14).

Zhang, X., Xu, Y., Qian, Z., Zheng, W., Wu, Q., Chen, Y., ... & Yu, Y. (2018). circRNA_104075 stimulates YAP-dependent tumorigenesis through the regulation of HNF4a and may serve as a diagnostic marker in hepatocellular carcinoma. Cell death & disease, 9(11), 1091.

Liu, J., Shen, Q., Li, G., & Xu, H. (2018). HNF4A-related Fanconi syndrome in a Chinese patient: a case report and review of the literature. Journal of medical case reports, 12(1), 1-5.

Qu, M., Duffy, T., Hirota, T., & Kay, S. A. (2018). Nuclear receptor HNF4A transrepresses CLOCK: BMAL1 and modulates tissue-specific circadian networks. Proceedings of the National Academy of Sciences, 115(52), E12305-E12312.

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

Custom Antibody Labeling

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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