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Mouse Anti-NFIB Antibody (1B5) (CBMAB-0723-YC)

Provided herein are mouse monoclonal antibodies against Human NFWB. The antibody clone 1B5 can be used for immunoassay techniques, such as ELISA and IP.
See all NFIB antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
1B5
Antibody Isotype
IgG2a
Application
ELISA, IP

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
NFIB
Introduction
NFIB (nuclear factor 1 B-type) is a transcription factor, which is a part of the NFI gene complex that includes three other genes (NFIA, NFIC and NFIX). NFIB has the highest concentrations in the lung, skeletal muscle and heart but is also found in the areas of the developing liver, kidneys and brain. NFIB is essential in embryonic development and it works together with its gene complex to initiate tissue differentiation in the fetus.
Entrez Gene ID
4781
UniProt ID
O00712
Alternative Names
NFI-RED; NFIB2; NFIB3
Function
Transcriptional activator of GFAP, essential for proper brain development (PubMed:30388402).
Recognizes and binds the palindromic sequence 5'-TTGGCNNNNNGCCAA-3' present in viral and cellular promoters and in the origin of replication of adenovirus type 2. These proteins are individually capable of activating transcription and replication.
Biological Process
Anterior commissure morphogenesisISS:UniProtKB
Brain developmentManual Assertion Based On ExperimentIMP:UniProtKB
Cell differentiation involved in salivary gland developmentIEA:Ensembl
Chondrocyte differentiationISS:UniProtKB
Club cell differentiationISS:UniProtKB
Commissural neuron axon guidanceISS:UniProtKB
DNA replicationIEA:UniProtKB-KW
Glial cell differentiationISS:UniProtKB
Hindbrain developmentIEA:Ensembl
Lung ciliated cell differentiationISS:UniProtKB
Negative regulation of DNA bindingIDA:UniProtKB
Negative regulation of epithelial cell proliferation involved in lung morphogenesisISS:UniProtKB
Negative regulation of mesenchymal cell proliferation involved in lung developmentISS:UniProtKB
Negative regulation of miRNA transcriptionManual Assertion Based On ExperimentIMP:BHF-UCL
Negative regulation of transcription by RNA polymerase IIIDA:UniProtKB
Positive regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of transcription, DNA-templatedManual Assertion Based On ExperimentIDA:UniProtKB
Principal sensory nucleus of trigeminal nerve developmentISS:UniProtKB
Regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIBA:GO_Central
Response to bacteriumIEA:Ensembl
Salivary gland cavitationIEA:Ensembl
Type I pneumocyte differentiationISS:UniProtKB
Type II pneumocyte differentiationISS:UniProtKB
Cellular Location
Nucleus
Involvement in disease
Macrocephaly, acquired, with impaired intellectual development (MACID):
An autosomal dominant disorder characterized by postnatal macrocephaly and borderline to mild mental retardation. Additional variable neurodevelopmental features include muscular hypotonia, motor and speech delay, attention deficit disorder, autism spectrum disorder, and behavioral abnormalities. Some patients present corpus callosum dysgenesis.

Campbell, C. E., Webber, K., Bard, J. E., Chaves, L. D., Osinski, J. M., & Gronostajski, R. M. (2024). Nuclear Factor IA (Nfia) and Nuclear Factor IB (Nfib) are jointly required for mouse postnatal neural stem cell self-renewal. Stem Cells and Development, (ja).

Zhang, W., Wang, Y., Liu, Y., Liu, C., Wang, Y., He, L., ... & Shang, Y. (2023). NFIB facilitates replication licensing by acting as a genome organizer. Nature Communications, 14(1), 5076.

Marinella, G., Conti, E., Buchignani, B., Sgherri, G., Pasquariello, R., Giordano, F., ... & Battaglia, A. (2023). Further characterization of NFIB‐associated phenotypes: Report of two new individuals. American Journal of Medical Genetics Part A, 191(2), 540-545.

Huang, H., Jin, J., Wu, L., Wu, H., Pi, H., Dong, Y., & Xiang, R. (2022). A de novo non-sense nuclear factor IB mutation (p. Tyr290*) is responsible for brain malformation and lung lobulation defects. Frontiers in Pediatrics, 10, 865181.

Sun, H., Li, N., Tan, J., Li, H., Zhang, J., Qu, L., & Lamont, S. J. (2022). Transcriptional regulation of RIP2 gene by NFIB is associated with cellular immune and inflammatory response to APEC infection. International journal of molecular sciences, 23(7), 3814.

Yu, J. G., Song, Y., Yang, A., Zhang, X., & Li, L. (2021). Serum nuclear factor IB as a novel and noninvasive indicator in the diagnosis of secondary hyperparathyroidism. Journal of Clinical Laboratory Analysis, 35(6), e23787.

Pan, D., Qian, B., Zhao, D., & Yao, B. (2021). Nfib promotes chondrocyte proliferation and inhibits differentiation by mildly regulating Sox9 and its downstream genes. Molecular Biology Reports, 48, 7487-7497.

Dasgupta, S., Ewing‑Graham, P. C., Van Den Bosch, T. P., Swagemakers, S., Santegoets, L. A., Van Doorn, H. C., ... & Van Kemenade, F. J. (2021). Nuclear factor IB is downregulated in vulvar squamous cell carcinoma (VSCC): Unravelling differentially expressed genes in VSCC through gene expression dataset analysis. Oncology Letters, 21(5), 1-11.

Barrus, K., Rego, S., Yip, T., Martin, P. M., Glen, O. A., Van Ziffle, J., & Slavotinek, A. M. (2020). The expanding spectrum of NFIB‐associated phenotypes in a diverse patient population—A report of two new patients. American Journal of Medical Genetics Part A, 182(12), 2959-2963.

Jain, S., Burchett, R., Monckton, E. A., & Godbout, R. (2019). A positive feedback loop involving nuclear factor IB and calpain 1 suppresses glioblastoma cell migration. Journal of Biological Chemistry, 294(34), 12638-12654.

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

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