Anti-GFI1B Antibody (C-term)

Product Name

Anti-GFI1B Antibody (C-term)

View all GFI1B Antibodies

SKU/Catalog Number

A03180

Size

80 µl

Description

Boster Bio Anti-GFI1B Antibody (C-term) (Catalog # A03180). Tested in WB application(s). This antibody reacts with Human, Mouse.

Storage & Handling

Maintain refrigerated at 2-8°C for up to 2 weeks. For long-term storage, store at -20°C in small aliquots to prevent freeze-thaw cycles.

Cite This Product

Anti-GFI1B Antibody (C-term) (Boster Biological Technology, Pleasanton CA, USA, Catalog # A03180)

Host

Rabbit

Contents

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide.

Clonality

Polyclonal

Isotype

Rabbit IgG

Immunogen

This GFI1B antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 302-330 amino acids from the C-terminal region of human GFI1B.

*Blocking peptide can be purchased. Costs vary based on immunogen length. Contact us for pricing.

Reactive Species

A03180 is reactive to GFI1B in Human, Mouse

Applications

A03180 is guaranteed for WB Boster Guarantee

Observed Molecular Weight

Calculated molecular weight

37492 Da

Background of GFI1B

Essential proto-oncogenic transcriptional regulator necessary for development and differentiation of erythroid and megakaryocytic lineages. Component of a RCOR-GFI-KDM1A-HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development and controls hematopoietic differentiation. Transcriptional repressor or activator depending on both promoter and cell type context; represses promoter activity of SOCS1 and SOCS3 and thus, may regulate cytokine signaling pathways. Cooperates with GATA1 to repress target gene transcription, such as the apoptosis regulator BCL2L1; GFI1B silencing in leukemic cell lines markedly increase apoptosis rate. Inhibits down-regulation of MYC and MYB as well as the cyclin-dependent kinase inhibitor CDKN1A/P21WAF1 in IL6-treated myelomonocytic cells. Represses expression of GATA3 in T-cell lymphomas and inhibits GATA1-mediated transcription; as GATA1 also mediates erythroid GFI1B transcription, both GATA1 and GFI1B participate in a feedback regulatory pathway controlling the expression of GFI1B gene in erythroid cells. Suppresses GATA1-mediated stimulation of GFI1B promoter through protein interaction. Binds to gamma-satellite DNA and to its own promoter, auto-repressing its own expression. Alters histone methylation by recruiting histone methyltransferase to target genes promoters. Plays a role in heterochromatin formation.

Antibody Validation

Boster validates all antibodies on WB, IHC, ICC, Immunofluorescence, and ELISA with known positive control and negative samples to ensure specificity and high affinity, including thorough antibody incubations.

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Assay Dilutions Recommendation

The recommendations below provide a starting point for assay optimization. The actual working concentration varies and should be decided by the user.

WB: 1:1000

Validation Images & Assay Conditions

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GFI1B Antibody (C-term) western blot analysis in HL-60,K562,U266
cell line and mouse spleen lysates (35ug/lane). This demonstrates the GFI1B antibody detected the GFI1B protein (arrow).

Gene/Protein Information For GFI1B (Source: Uniprot.org, NCBI)

Alternative Names

growth factor independent 1B transcription repressor; Growth factor independent protein 1B; Potential regulator of CDKN1A translocated in CML; translocated inCML); zinc finger protein Gfi-1b GFI1B BDPLT17, ZNF163B growth factor independent 1B transcriptional repressor zinc finger protein Gfi-1b|growth factor independent 1B (potential regulator of CDKN1A, translocated in CML)|growth factor independent 1B transcription repressor

For more info on GFI1B, check out the GFI1B Infographic

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In this infographic, you will see the following information for GFI1B: database IDs, superfamily, protein function, synonyms, molecular weight, chromosomal locations, tissues of expression, subcellular locations, post-translational modifications, and related diseases, research areas & pathways. If you want to see more information included, or would like to contribute to it and be acknowledged, please contact [email protected].

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