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Mouse Anti-PAX4 Recombinant Antibody (CBT3746) (V2LY-0625-LY2575)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBT3746
Antibody Isotype
IgG1
Application
WB

Basic Information

Immunogen
Purified recombinant fragment of human PAX4 expressed in E. Coli.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal Antibody
Application Notes
ApplicationNote
WB1:500-1:2,000
ELISA1:10,000

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

Format
Supernatant
Preservative
Sodium azide
Concentration
Batch dependent
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
Paired Box 4
Entrez Gene ID
5078
UniProt ID
O43316
Function
Plays an important role in the differentiation and development of pancreatic islet beta cells. Transcriptional repressor that binds to a common element in the glucagon, insulin and somatostatin promoters. Competes with PAX6 for this same promoter binding site. Isoform 2 appears to be a dominant negative form antagonizing PAX4 transcriptional activity.
Biological Process
Anatomical structure developmentManual Assertion Based On ExperimentIBA:GO_Central
Animal organ morphogenesisManual Assertion Based On ExperimentTAS:ProtInc
Cell differentiationIEA:UniProtKB-KW
Pancreas developmentIEA:InterPro
Regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Cellular Location
Nucleus
Involvement in 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.
Diabetes mellitus, insulin-dependent (IDDM):
A multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical features are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.
Diabetes mellitus, ketosis-prone (KPD):
An atypical form of diabetes mellitus characterized by an acute initial presentation with severe hyperglycemia and ketosis, as seen in classic type 1 diabetes, but after initiation of insulin therapy, prolonged remission is often possible with cessation of insulin therapy and maintenance of appropriate metabolic control. Metabolic studies show a markedly blunted insulin secretory response to glucose, partially reversible with the improvement of blood glucose control. Variable levels of insulin resistance are observed, especially in obese patients. Pancreatic beta-cell autoimmunity is a rare finding.
Maturity-onset diabetes of the young 9 (MODY9):
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.
More Infomation

Teerawattanapong, N., Srisawat, L., Narkdontri, T., Yenchitsomanus, P. T., Tangjittipokin, W., & Plengvidhya, N. (2024). The effects of transcription factor 7-like 2 rs7903146 and paired box 4 rs2233580 variants associated with type 2 diabetes on the therapeutic efficacy of hypoglycemic agents. Heliyon.

Ko, J., Fonseca, V. A., & Wu, H. (2023). Pax4 in health and diabetes. International Journal of Molecular Sciences, 24(9), 8283.

Kamal, M. M., Islam, M. N., Rabby, M. G., Zahid, M. A., & Hasan, M. M. (2023). In Silico Functional and Structural Analysis of Non-synonymous Single Nucleotide Polymorphisms (nsSNPs) in Human Paired Box 4 Gene. Biochemical Genetics, 1-24.

Narayan, G., Agrawal, A., Sen, P., Nagotu, S., & Thummer, R. P. (2023). Production of Bioactive Human PAX4 Protein from E. coli. The Protein Journal, 42(6), 766-777.

Lee, Y. L., Ting, T. H., Lim, C. T., Arrumugam-Arthini, C., Karuppiah, T., & Ling, K. H. (2023). Novel PAX4 variant in a child and family with diabetes mellitus–case report and review of the literature. Journal of Pediatric Endocrinology and Metabolism, 36(10), 988-992.

Zhang, D., Chen, C., Yang, W., Piao, Y., Ren, L., & Sang, Y. (2022). C. 487C> T mutation in PAX4 gene causes MODY9: A case report and literature review. Medicine, 101(51), e32461.

Zhang, Y., Ding, L., Ni, Q., Tao, R., & Qin, J. (2021). Transcription factor PAX4 facilitates gastric cancer progression through interacting with miR-27b-3p/Grb2 axis. Aging (Albany NY), 13(12), 16786.

Zhang, T., Wang, H., Wang, T., Wei, C., Jiang, H., Jiang, S., ... & Ma, L. (2019). Pax4 synergistically acts with Pdx1, Ngn3 and MafA to induce HuMSCs to differentiate into functional pancreatic β‑cells. Experimental and therapeutic medicine, 18(4), 2592-2598.

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

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