Datasheet

生物学的記述

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

Specificity

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

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.

使用情報

Application

WB, IP, IHC, IF, FCM

Dilution

Reactivity

Human

Source

Rabbit Monoclonal Antibody

MW

29 kDa

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

プロトコール

References

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

Application Data

WB

Validated by Selleck

Lane 1: Raji, Lane 2: Daudi, Lane 3: HDLM-2