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Mouse Anti-FOXN1 Recombinant Antibody (CBXF-2112) (CBMAB-F1067-CQ)

This product is a mouse antibody that recognizes FOXN1. The antibody CBXF-2112 can be used for immunoassay techniques such as: ELISA, WB.
See all FOXN1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXF-2112
Antibody Isotype
IgG1
Application
ELISA, WB

Basic Information

Specificity
Human
Antibody Isotype
IgG1
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!]

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
Forkhead Box N1
Introduction
Mutations in the winged-helix transcription factor gene at the nude locus in mice and rats produce the pleiotropic phenotype of hairlessness and athymia, resulting in a severely compromised immune system. This gene is orthologous to the mouse and rat genes and encodes a similar DNA-binding transcription factor that is thought to regulate keratin gene expression. A mutation in this gene has been correlated with T-cell immunodeficiency, the skin disorder congenital alopecia, and nail dystrophy. Alternative splicing in the 5' UTR of this gene has been observed.
Entrez Gene ID
8456
UniProt ID
O15353
Alternative Names
Forkhead Box N1; Winged-Helix Transcription Factor Nude; Winged-Helix Nude; Rowett Nude; RONU; WHN; Forkhead Box Protein N1; FKHL20;
Function
Transcriptional regulator which regulates the development, differentiation, and function of thymic epithelial cells (TECs) both in the prenatal and postnatal thymus. Acts as a master regulator of the TECs lineage development and is required from the onset of differentiation in progenitor TECs in the developing fetus to the final differentiation steps through which TECs mature to acquire their full functionality. Regulates, either directly or indirectly the expression of a variety of genes that mediate diverse aspects of thymus development and function, including MHC Class II, DLL4, CCL25, CTSL, CD40 and PAX1. Regulates the differentiation of the immature TECs into functional cortical TECs (cTECs) and medullary TECs (mTECs). Essential for maintenance of mTECs population in the postnatal thymus. Involved in the morphogenesis and maintenance of the three-dimensional thymic microstructure which is necessary for a fully functional thymus. Plays an important role in the maintenance of hematopoiesis and particularly T lineage progenitors within the bone marrow niche with age. Essential for the vascularization of the thymus anlage. Promotes the terminal differentiation of epithelial cells in the epidermis and hair follicles, partly by negatively regulating the activity of protein kinase C (By similarity).

Plays a crucial role in the early prenatal stages of T-cell ontogeny (PubMed:21507891).
Biological Process
Animal organ morphogenesis Source: ProtInc
Blood vessel morphogenesis Source: Ensembl
Defense response Source: ProtInc
Epidermis development Source: ProtInc
Hair follicle development Source: Ensembl
Keratinocyte differentiation Source: Ensembl
Lymphoid lineage cell migration into thymus Source: Ensembl
Nail development Source: Ensembl
Positive regulation of epithelial cell differentiation Source: BHF-UCL
Positive regulation of hair follicle development Source: Ensembl
Regulation of positive thymic T cell selection Source: Ensembl
Regulation of transcription by RNA polymerase II Source: GO_Central
T cell homeostasis Source: Ensembl
T cell lineage commitment Source: Ensembl
Thymus epithelium morphogenesis Source: Ensembl
Cellular Location
Nucleus
Involvement in disease
T-cell immunodeficiency, congenital alopecia, and nail dystrophy (TIDAND):
A disorder characterized by the association of congenital alopecia, severe T-cell immunodeficiency, and ridging and pitting of all nails.
T-cell lymphopenia, infantile, with or without nail dystrophy, autosomal dominant (TLIND):
n autosomal dominant disorder characterized by decreased numbers of T cells, particularly cytotoxic CD8+ T cells, and increased susceptibility to recurrent infections, mainly respiratory viral infections. Additional features may include impaired thymic development, skin abnormalities, such as atopic dermatitis, and nail dystrophy.
T-cell immunodeficiency with thymic aplasia (TIDTA):
An autosomal recessive disorder characterized by selective hypo- or aplasia of the thymus, T-cell immunodeficiency due to impaired T-cell development, and increased susceptibility to viral infections.

Kadouri, N., Givony, T., Nevo, S., Hey, J., Ben Dor, S., Damari, G., ... & Abramson, J. (2022). Transcriptional regulation of the thymus master regulator Foxn1. Science Immunology, 7(74), eabn8144.

Machcinska, S., Walendzik, K., Kopcewicz, M., Wisniewska, J., Rokka, A., Pääkkönen, M., ... & Gawronska‐Kozak, B. (2022). Hypoxia reveals a new function of Foxn1 in the keratinocyte antioxidant defense system. The FASEB Journal, 36(8), e22436.

McClure, M. J., Olson, L. C., Cohen, D. J., Huang, Y. C., Zhang, S., Nguyen, T., ... & Schwartz, Z. (2021). RNU (Foxn1 RNU-Nude) rats demonstrate an improved ability to regenerate muscle in a volumetric muscle injury compared to Sprague Dawley rats. Bioengineering, 8(1), 12.

Walendzik, K., Kopcewicz, M., Bukowska, J., Panasiewicz, G., Szafranska, B., & Gawronska-Kozak, B. (2020). The transcription factor FOXN1 regulates skin adipogenesis and affects susceptibility to diet-induced obesity. Journal of Investigative Dermatology, 140(6), 1166-1175.

Gawronska-Kozak, B. (2020). Foxn1 control of skin function. Applied Sciences, 10(16), 5685.

Oh, J., Wang, W., Thomas, R., & Su, D. M. (2020). Thymic rejuvenation via FOXN1-reprogrammed embryonic fibroblasts (FREFs) to counteract age-related inflammation. JCI insight, 5(18).

Bosticardo, M., Yamazaki, Y., Cowan, J., Giardino, G., Corsino, C., Scalia, G., ... & Notarangelo, L. D. (2019). Heterozygous FOXN1 variants cause low TRECs and severe T cell lymphopenia, revealing a crucial role of FOXN1 in supporting early thymopoiesis. The American Journal of Human Genetics, 105(3), 549-561.

Du, Q., Huynh, L. K., Coskun, F., Molina, E., King, M. A., Raj, P., ... & van Oers, N. S. (2019). FOXN1 compound heterozygous mutations cause selective thymic hypoplasia in humans. The Journal of Clinical Investigation, 129(11), 4724-4738.

Bukowska, J., Kopcewicz, M., Walendzik, K., & Gawronska-Kozak, B. (2018). Foxn1 in skin development, homeostasis and wound healing. International Journal of Molecular Sciences, 19(7), 1956.

Kur-Piotrowska, A., Bukowska, J., Kopcewicz, M. M., Dietrich, M., Nynca, J., Slowinska, M., & Gawronska-Kozak, B. (2018). Foxn1 expression in keratinocytes is stimulated by hypoxia: Further evidence of its role in skin wound healing. Scientific reports, 8(1), 1-14.

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

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