SMARCB1 Antibodies

SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMARCB1)

Core part of the BAF (hSWI/SNF) complicated. This ATP- dependent chromatin-remodeling complicated plays important roles in cell proliferation and differentiation, in cellular antiviral activities and inhibition of tumor formation.

The BAF complex is able to make a stable, altered form of chromatin that constrains fewer negative supercoils than normal. This change in supercoiling would be due to the conversion of around one-half of the nucleosomes on polynucleosomal arrays into asymmetric structures, termed altosomes, each composed of 2 histones octamers.

Gene Information

Human
Gene Name:	SMARCB1
Uniprot:	Q12824
Entrez:	6598

Family

Belongs to:
SNF5 family

Alternative Names

BAF47; BAF47hSNF5; BRG1-associated factor 47; hSNFS; Ini1; INI1RTPS1; Integrase interactor 1 protein; malignant rhabdoid tumor suppressor; RDTSNF5 homolog; Sfh1p; SNF5; SNF5L1; Snr1; subfamily b, member 1; sucrose nonfermenting, yeast, homolog-like 1; SWI/SNF related, matrix associated, actin dependent regulator of chromatin; SWI/SNF-related matrix-associated actin-dependent regulator of chromatinsubfamily B member 1

Molecular Weight

Mass (kDA):
44.141 kDA

Genomic Context

Human
Location:	22q11.23|22q11
Sequence:	22; NC_000022.11 (23786966..23838009)

Subcellular Localizations

Nucleus.

Diseases

• Neoplasms
• Rhabdoid Tumor
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasms
• Brain Neoplasms
• Atypical Teratoid/rhabdoid Tumor
• Nervousness
• Teratoma
• Sarcoma
• Carcinoma
• Cell Transformation, Neoplastic
• Neurilemmoma
• Schwannomatosis

• Kidney Neoplasm
• Neurofibromatosis 2
• Central Nervous System Neoplasms
• Epithelioid Sarcoma
• Neoplasm Metastasis
• Medulloblastoma
• Meningioma

Interacting Proteins

• ARID2
• CALR
• SMARCA4
• Smarca4

Pathways

• Chromatin Remodeling
• Cell Cycle
• Pathogenesis
• Atp-dependent Chromatin Remodeling
• Cell Cycle Arrest
• Cell Growth
• Cell Proliferation
• Senescence
• Oncogenesis
• Rna Interference
• Methylation
• Reverse Transcription

• Viral Replication
• Dna Replication
• Regulation Of Gene Expression
• Localization
• Nuclear Export
• Gene Silencing
• S Phase

PTMs

• Phosphorylation
• Methylation
• Acetylation

• Dephosphorylation
• Cleavage
• Deacetylation

• Ubiquitination

Research Areas

• Cell Cycle and Replication

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SMARCB1

Boster Bio: Best Uses Of The SMARCB1 Marker

If you are interested in immunohistochemistry, you may want to check out this SMARCB1 primer and antibody. This primer is specifically designed for immunohistochemistry, and it enables you to visualize and analyze the SMARCB1 protein in tissues. Before you use the primer, it is important to understand how to apply, priming, and incubate.

SMARCB1 immunohistochemistry

In recent years, the use of SMARCB1 immunohistochemistry has expanded to include pediatric neoplasms. This new immunohistochemistry technique can be used to detect SMARCB1 protein expression in lung tumors. This type of tumor occurs mostly in middle-aged to young adults. It is strongly linked with a history and practice of smoking. Some patients are diagnosed with SMARCB1 -deficient squamous cancer.

During these studies, the use of SMARCB1 immunohistochemistry revealed that it was expressed primarily in germinal center B cells. This cell type displayed granular staining in the cytoplasm. This cellular kind was not present in the Ewing’s sarcoma cell-line (ES1).

SMARCB1 immunohistochemistry is performed using a mouse model. It shows that the protein can be found in many complexes. It is part of the Emerin regulatory compound. This complex is implicated in redox metabolism and is associated with cancer risk. It also contributes to NSP'G1's role in ribosome biogenesis and cancer risk.

Gcet1+ lymphocytes are found in the germinal and marginal zones of lymphocyte differentiation. Gcet1 immunohistochemistry reveals a cytoplasmic location, while some Burkitt lymphoma patients are negative for this marker. These cases show immunohistochemical patterns that are similar to LRCHL. Further studies are required to clarify the biological significance of Gcet1 expression.

Applications

The SMARCB1 genome encodes a protein. SMARCB1 is a subunit of the SWI/SNF protein complex, which regulates gene expression and activity. SMARCB1 is important for regulating chromatin remodeling, a process that alters the tightness of DNA packaging. Chromatin remodelling plays an important role during development in controlling gene expression.

Although the exact role SMARCB1 may play in cancer research remains unknown, it has been shown in the regulation the immune response. SMARCB1 could prevent or delay cancer development by inhibiting IL6. SMARCB1 genes can detect a tumour before it progresses. SMARCB1 can also be associated with asthma and other inflammation-related diseases.

SMARCB1 has been identified to be a tumor suppressor gene. It has been genetically mutated in many cancers, including those of liver, kidney, and brain. It regulates cell cycle regulation and suppresses transcription of the mammalian C-MYC gene. It also regulates positioning of nucleosomes.

Recent SWI/SNF studies have shown that SMARCB1 mutants are rare. SMARCB1 mutants have been identified in a variety cancers, including teratoid/rhabdoid. Multiple changes can occur within a single cells when SMARCB1 mutations are inactivated. A study of a patient suffering from rare regional inactivation (SMARCB1) revealed that a spontaneous regression of a teratoid/rhabdoid tumour was also possible without treatment.

Recent research has shown that schwannoma is predisposed to a number SMARCB1 variants. Initially, this gene was identified in the context of atypical teratoid/rhabdoid tumours. These tumours often strike young children and can kill before age three. Multiple recurrences can also be associated with SMARCB1 variants.

A study on immortalized human cell lines further examined the role SMARCB1 plays in the cell cycle. Knockdowns of SMARCB1 resulted in a decrease in cell cycle progression and an increase in p21. These findings suggest that SMARCB1 regulates several genes associated with cell maintenance, inflammation, and cellular metabolism. SMARCB1 is also involved in immune response, inflammation, and immune response.

Primers

Boster Bio: Nature Communications published a new paper titled Best Uses of SMARCA4 to detect SMARCB1 gene expression within human cancer cells. This study found SMARCA4 to be significantly enriched in human tumors. SMARCA4 has a positive correlation with TGFB expression and is highly expressed in basal-like tumours.

The SMARCB1 gene was extensively studied in cancer cell lines and in the SMARCB1 chromosome. Boster was the first to discover the gene in 1993. The company quickly developed products that could detect SMARCB1 in cell lines. It also produced hundreds of primary antibodies. During the 1990s, Boster Bio became the largest catalog antibody company in China. PicoKine(tm), Boster Bio's proprietary ELISA platform, was developed. It uses trade secrets to create high-sensitivity ELISA kit kits.

The SMARCA4 gene expression is highly correlated with SMARCA4 activity. This marker is able to detect SMARCA4 expression when it is co-expressed with SOX4. SMARCA4 belongs to the SWI/SNF subunit of the ATPase family. It is found to be expressed more in basal-like cells of breast cancer. Its expression correlates with SMARCA4 gene and SMARCD2 genes.

Incubation

The study included 100 rhabdoid tumour patients to determine the prevalence of germline SMARCB1 defects. The majority of these cases had mutations or concomitant deletions of the SMARCB1 gene. MLPA, direct sequencing, and SNP array analysis are all methods that can be used to detect germline SMARCB1 abnormalities. Patients with mutations or deletions can be predisposed to the disease in any body part; however, they exhibit variable expression and penetrance.

Patients with rhabdoid sarcomas at different sites have a high chance of developing germline SMARCB1 abnormalities. These tumors could represent metastases or distinct secondary hits. This is especially true for patients who have multiple primary tumours. Similar patterns have been observed in children who have sporadic rhabdoid cancers. Although these cases were not associated a priori with rhabdoid cancers, the families of both patients as well as their parents suggested that the mutation may have occurred de novo.

The top genes of this signature map to the long arm of chromosome 22. The gene is high-expressing in the early stages. It is associated with a poorer outlook than patients with germline SMARCB1 genetic mutations. Patients with germline SMARCB1 variants are typically younger and more susceptible to developing cancer. This genetic variant can increase your risk of developing melanomas.

Moreover, SMARCB1 deletions at embryonic day E6 –E7 lead to highly pervasive CNS tumors. However, deletions of the gene at later times have little or no effect. This may be due to an undifferentiated state that is necessary for tumorigenesis. Reintroduction SMARCB1 reveals widespread recruiting of SWI/SNF to enhancers, activation and resolution of bivalency.

Vimentin was strongly associated with tumors that had SMARCB1/INI1 gene expression. However, tumors with p53 or CIMP expression were not associated with SMARCB1/INI1-high tumors. Cell cycle instability may also explain the loss these genes. Low levels of this protein in tumors were also more likely to be poorly differentiated or have liver metastasis.