FLNB Antibodies

Structure of FLNB

Filamentin B encoded by the FLNB gene is a high-molecular-weight cytoskeletal protein with a molecular weight of approximately 280 kDa. There are certain structural differences among different species:

The FLNB protein is composed of 2,647 amino acids and has a dimer structure, interacting with the cytoskeleton through its N-terminal actin binding domain. This protein contains 24 repetitive immunoglobulin (Ig) -like domains, forming a flexible V-shaped conformation that endows it with mechanical sensing capabilities.

Fig. 1 Schematic of FLNB (Filamin B) protein domain structure.¹

Key structural properties of FLNB:

• Multi-domain flexible configuration
• Mechanically sensitive hinge area
• Actin cross-linking site
• Signal molecule binding domain

Functions of FLNB

FLNB protein, as a key regulatory factor of the cytoskeleton, mainly participates in the maintenance of cell morphology and mechanical signal transduction, and also plays an important role in various physiological and pathological processes.

Compared with other members of the filamentin family (FLNA/FLNC), FLNB has a unique developmental stage-specific expression pattern. The loss of its function can lead to more severe skeletal system defects. This protein forms a V-type dimer through the dimerization domain at the C-terminal. This special conformation enables it to simultaneously integrate mechanical stimuli and biochemical signals, playing an irreplaceable role in tissue development and homeostasis maintenance.

Applications of FLNB and FLNB Antibody in Literature

1. Fan, Guoyong, et al. "FLNB overexpression promotes tumor progression and associates with immune suppression, evasion and stemness in pancreatic cancer." American Journal of Cancer Research 14.2 (2024): 709. https://europepmc.org/article/med/38455418

This study, through bioinformatics analysis and experimental verification, found that filicin B (FLNB) is highly expressed in pancreatic cancer and is associated with a poor prognosis. FLNB promotes tumor progression by regulating the cell cycle, angiogenesis and immunosuppressive microenvironment (such as promoting Treg cell and TAMs infiltration and inhibiting CD8+ T cells), and may become a new target for the treatment of pancreatic cancer.

2. Fukushima, Kaya, et al. "Intragenic deletions in FLNB are part of the mutational spectrum causing spondylocarpotarsal synostosis syndrome." Genes 12.4 (2021): 528. https://doi.org/10.3390/genes12040528

Research has found that novel homozygous deletion mutations of the FLNB gene (c.1346-1372_1941+389del and c.3127-353_4223-1836del) can lead to spinal-carpal tarsal fusion syndrome (SCT), and for the first time confirmed that large fragment structural variations of FLNB are related to this disease. It is recommended to adopt copy number detection to improve the molecular diagnostic rate of SCT.

3. Veyssiere, Maëva, et al. "MYLK* FLNB and DOCK1* LAMA2 gene–gene interactions associated with rheumatoid arthritis in the focal adhesion pathway." Frontiers in genetics 15 (2024): 1375036.https://doi.org/10.3389/fgene.2024.1375036

Research has found that the rare interaction between the FLNB and MYLK genes can increase the risk of rheumatoid arthritis (RA). Through whole exome sequencing and MB-MDR analysis, it was revealed for the first time that FLNB is involved in the plaque adhesion pathway and promotes the occurrence of RA through gene interaction (MYLK*FLNB), providing new insights into the genetic mechanism of RA.

4. Ni, Lina, et al. "The expression and prognostic value of disulfidptosis progress in lung adenocarcinoma." Aging (Albany NY) 15.15 (2023): 7741.https://doi.org/10.18632/aging.204938

Based on the TCGA and GEO databases, this study constructed a prognostic model for lung adenocarcinoma containing five disulfide bond death-related genes (ACTB, FLNB, NCKAP1, SLC3A2, SLC7A11), including FLNB. Single-cell sequencing revealed that FLNB and NCKAP1 were highly expressed in endothelial cells. This model has higher predictive efficacy than clinical parameters, providing a new tool for the prognosis assessment of lung adenocarcinoma.

5. Li, Ji, et al. "An alternative splicing switch in FLNB promotes the mesenchymal cell state in human breast cancer." Elife 7 (2018): e37184. https://doi.org/10.7554/eLife.37184

Research has found that RNA-binding proteins QKI and RBFOX1 induce epithelial-mesenchymal transition (EMT) by regulating the alternative splicing of FLNB exon 30, which promotes the release of the FOXC1 transcription factor by FLNB splicing variants. Abnormal FLNB splicing is significantly associated with the EMT characteristics of basal-like breast cancer, revealing a new regulatory mechanism of tumor cell plasticity.

Creative Biolabs: FLNB Antibodies for Research

Creative Biolabs specializes in the production of high-quality FLNB antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom FLNB Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our FLNB antibodies, custom preparations, or technical support, contact us at email.