WH0002672M1
Monoclonal Anti-GFI1 antibody produced in mouse
clone 3G8, purified immunoglobulin, buffered aqueous solution
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All Photos(5)
Synonym(s):
Anti-ZNF163, Anti-growth factor independent 1
Recommended Products
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
3G8, monoclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
indirect ELISA: suitable
indirect immunofluorescence: suitable
western blot: 1-5 μg/mL
isotype
IgG1κ
GenBank accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... GFI1(2672)
General description
Growth factor independent protein 1 (GFI1) is a zinc finger DNA-binding protein with an N-terminal SNAIL/Gfi-1 (SNAG) domain and C-terminal Zinc finger motifs. The GFI1 gene is mapped to human chromosome 1p22.1.
Immunogen
GFI1 (NP_005254, 1 a.a. ~ 91 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Sequence
MPRSFLVKSKKAHSYHQPRSPGPDYSLRLENVPAPSRADSTSNAGGAKAEPRDRLSPESQLTEAPDRASASPRQLRSSVCERSSEFEDFWR
Sequence
MPRSFLVKSKKAHSYHQPRSPGPDYSLRLENVPAPSRADSTSNAGGAKAEPRDRLSPESQLTEAPDRASASPRQLRSSVCERSSEFEDFWR
Biochem/physiol Actions
Growth factor independent protein 1 (GFI1) regulates lymphomagenesis and differentiation of hematopoietic and non-hematopoietic tissues especially those associated with lungs, intestine, and inner ear hair cells. It acts as a transcriptional repressor protein that recruits histone demethylase complex (LSD-1) and histone deacetylases. Gfi1 serves as a mediator of the cell cycle and apoptosis. It favors multiple myeloma tumor progression and chemoresistance. Mutation in the GFI1 gene is implicated in severe congenital neutropenia (SCN).
Physical form
Solution in phosphate buffered saline, pH 7.4
Legal Information
GenBank is a registered trademark of United States Department of Health and Human Services
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Regulatory Information
常规特殊物品
Certificates of Analysis (COA)
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Eduardo Anguita et al.
Frontiers in oncology, 7, 54-54 (2017-04-13)
Many human diseases arise through dysregulation of genes that control key cell fate pathways. Transcription factors (TFs) are major cell fate regulators frequently involved in cancer, particularly in leukemia. The GFI1B gene, coding a TF, was identified by sequence homology
Ji Un Kang et al.
International journal of oncology, 36(6), 1429-1435 (2010-04-30)
Homozygous deletions (HDs) are major genomic forces contributing to the development of many solid tumors. To identify critical tumor-suppressor loci involved in the pathogenesis of gastric carcinoma (GC), a high-resolution microarray-CGH was performed in a series of 27 GC patients.
Nadia Ashour et al.
International journal of molecular sciences, 21(13) (2020-07-08)
Prostate and breast cancer constitute the most common cancers among men and women worldwide. The aging population is one of the main risk factors for prostate and breast cancer development and accumulating studies link aging with epigenetic changes. Growth factor
Daniela N Petrusca et al.
Journal of hematology & oncology, 11(1), 123-123 (2018-10-06)
In spite of major advances in treatment, multiple myeloma (MM) is currently an incurable malignancy due to the emergence of drug-resistant clones. We previously showed that MM cells upregulate the transcriptional repressor, growth factor independence 1 (Gfi1), in bone marrow
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