SPIB Antibody [F10D9] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution

Application
WB, IP, IHC, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
29 kDa 46 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
SPIB Antibody [F10D9] detects endogenous levels of total SPIB protein.

Clone
F10D9

Synonym(s)
Transcription factor Spi-B, SPIB

Background
Spi-B (SPIB) is a lymphoid-enriched ETS family transcription factor that binds purine-rich PU-box elements with the core sequence GAGGAA and functions as a sequence-specific transcriptional activator in immune and stromal compartments of lymphoid organs. The protein contains a C‑terminal ETS DNA-binding domain that mediates high-affinity recognition of PU-box motifs and an N‑terminal transactivation region that engages the transcriptional machinery and cooperates with partner factors on composite regulatory elements in target promoters and enhancers. SPIB is expressed in B-lineage cells, including germinal center and memory B cells, in plasmacytoid dendritic cells, and in fibroblastic reticular cells (FRCs) in lymph nodes, and regulates transcriptional programs that maintain B-cell identity, support humoral memory, and organize lymphoid stromal networks. SPIB promotes expression of B-cell–related genes, maintains expression of transcription factors that preserve the memory B-cell state, and limits terminal plasma cell differentiation by sustaining regulators such as Bach2 and restraining Blimp1, thereby supporting the longevity and survival of memory B cells and maintaining the pool of antigen-experienced cells. SPIB also controls the expression of components of the B-cell receptor (BCR) signaling cascade and NF‑κB pathway, placing this factor as a link between antigen receptor signaling and transcriptional control of B-cell fate decisions, including the balance between memory maintenance and plasma cell generation. In lymph node FRCs, SPIB is required for normal organization of the reticular network in T-cell zones and regulates expression of key niche factors such as CCL21 and interleukin‑7, thereby influencing CD8⁺ T-cell positioning, survival signals, and the magnitude of antiviral effector responses during infection. SPIB participates in the development and function of mucosal M cells in intestinal Peyer’s patches, contributes to plasmacytoid dendritic cell type I interferon responses through binding to interferon gene regulatory regions, and forms part of the broader SPI1/SPIB ETS subfamily that partitions transcriptional control across B cells, dendritic cells, and stromal elements. Altered SPIB expression or activity associates with defects in memory B-cell maintenance and germinal center responses, with impaired lymph node stromal architecture and weakened CD8⁺ T-cell immunity, and with selected lymphoid malignancies in which SPIB affects proliferation, survival, and cytokine or chemokine expression profiles.

Background

Spi-B (SPIB) is a lymphoid-enriched ETS family transcription factor that binds purine-rich PU-box elements with the core sequence GAGGAA and functions as a sequence-specific transcriptional activator in immune and stromal compartments of lymphoid organs. The protein contains a C‑terminal ETS DNA-binding domain that mediates high-affinity recognition of PU-box motifs and an N‑terminal transactivation region that engages the transcriptional machinery and cooperates with partner factors on composite regulatory elements in target promoters and enhancers. SPIB is expressed in B-lineage cells, including germinal center and memory B cells, in plasmacytoid dendritic cells, and in fibroblastic reticular cells (FRCs) in lymph nodes, and regulates transcriptional programs that maintain B-cell identity, support humoral memory, and organize lymphoid stromal networks. SPIB promotes expression of B-cell–related genes, maintains expression of transcription factors that preserve the memory B-cell state, and limits terminal plasma cell differentiation by sustaining regulators such as Bach2 and restraining Blimp1, thereby supporting the longevity and survival of memory B cells and maintaining the pool of antigen-experienced cells. SPIB also controls the expression of components of the B-cell receptor (BCR) signaling cascade and NF‑κB pathway, placing this factor as a link between antigen receptor signaling and transcriptional control of B-cell fate decisions, including the balance between memory maintenance and plasma cell generation. In lymph node FRCs, SPIB is required for normal organization of the reticular network in T-cell zones and regulates expression of key niche factors such as CCL21 and interleukin‑7, thereby influencing CD8⁺ T-cell positioning, survival signals, and the magnitude of antiviral effector responses during infection. SPIB participates in the development and function of mucosal M cells in intestinal Peyer’s patches, contributes to plasmacytoid dendritic cell type I interferon responses through binding to interferon gene regulatory regions, and forms part of the broader SPI1/SPIB ETS subfamily that partitions transcriptional control across B cells, dendritic cells, and stromal elements. Altered SPIB expression or activity associates with defects in memory B-cell maintenance and germinal center responses, with impaired lymph node stromal architecture and weakened CD8⁺ T-cell immunity, and with selected lymphoid malignancies in which SPIB affects proliferation, survival, and cytokine or chemokine expression profiles.

References
https://pubmed.ncbi.nlm.nih.gov/1406622/ https://pubmed.ncbi.nlm.nih.gov/37965309/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%