Sin3a Antibodies

Paired amphipathic helix protein Sin3a (Sin3a)

Acts as a transcriptional repressor. Corepressor for REST.

Interacts with MXI1 to repress MYC responsive genes and antagonize MYC oncogenic activities. Also interacts with MXD1-MAX heterodimers to repress transcription by tethering SIN3A to DNA.

Gene Information

Mouse
Gene Name:	Sin3a
Uniprot:	Q60520
Entrez:	20466

Family

Belongs to:
No superfamily

Alternative Names

DKFZp434K2235; FLJ90319; Histone deacetylase complex subunit Sin3a; KIAA0700; paired amphipathic helix protein Sin3a; SIN3 homolog A, transcription regulator (yeast); SIN3 homolog A, transcriptional regulator (yeast); SIN3A; Transcriptional corepressor Sin3a; transcriptional co-repressor Sin3A; transcriptional regulator, SIN3A

Molecular Weight

Mass (kDA):
145.088 kDA

Genomic Context

Mouse
Location:	9 B|9 30.89 cM
Sequence:	9;

Tissue Specificity

Widely expressed. Highest levels in testis, lung and thymus.

Diseases

• Neoplasms
• Malignant Neoplasms
• Cell Transformation, Neoplastic
• Leukemia
• Sudden Infant Death Syndrome
• Rett Syndrome
• Malignant Neoplasm Of Breast
• Metabolic Bone Disorder
• Autistic Disorder
• Traditional Serrated Adenoma
• Mammary Neoplasms
• Hyperplasia

• Myeloid Leukemia
• Nervousness
• Immunologic Deficiency Syndromes
• Sterility
• Acute Leukemia
• Chromosomal Translocation

Pathways

• Methylation
• Chromatin Remodeling
• Cell Cycle
• Dna Methylation
• Localization
• Gene Silencing
• Histone Acetylation
• Cell Growth
• Histone Deacetylation
• Cell Proliferation
• Regulation Of Gene Expression
• Cell Differentiation
• Demethylation

• Chromatin Modification
• Atp-dependent Chromatin Remodeling
• Translation
• Embryo Development
• Chromatin Organization
• Dna Repair
• Stem Cell Differentiation

PTMs

• Methylation
• Acetylation
• Deacetylation
• Phosphorylation
• Demethylation

• Sumoylation
• Reduction
• Hydroxylation
• Cleavage
• Dephosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Sin3a

Best Uses Of The SIN3A Marker By Boster Bio

Antibodies to SIN3A have many uses. The BosterBio Anti–SIN3A Antibody has been evaluated in immunofluorescence as well as ChIP, IP, IIF, IF and WB. Continue reading to learn more about the benefits this antibody can bring to your research. We'll also talk about the drawbacks and advantages of this product.

Boster Bio Anti-SIN3A Marker

Boster Bio offers the anti-SIN3A marker in a variety formats, including Western Blotting and ELISA. It reacts well with Humans and can be stored at 20°C for a year. It is also available as a liquid in 50% glycerol/0.02% nitrate. BosterBio Anti-SIN3A has been tested for specificity & accuracy for Western Blotting.

The anti-SIN3A indicator recognizes the presence Listeria species like Carnobacterium.sp., Desulfonatronum.thidismutans (DSM-4847), Opitutaceae.bacterium TAV5 and Leptotrichia wadei. It also identifies several Leptotrichia strains, including its most widely distributed.

MiR-210-3p directly targets SIN3A

It is not clear which function miR210-3p has in lung cancer. It is linked to a decrease of lung cancer tissues and adjacent tissue, and an increase of miR-210-3p. Furthermore, miR-210-3p regulates the expression of SIN3A in lung cancer tissue. This microRNA could thus be a potential therapeutic target in NSCLC treatment.

To investigate whether miR-210-3p directly targets SIN3, we used a dual-luciferase reporter assay. Comparing to the control condition miR-210-3p significantly suppressed SIN3A-3’UTR reporter activities, whereas they did no harm to the SIN3A–MUT reporter. Our results showed that miR-210-3p may be an effective therapeutic agent for SIN3A.

Overexpression of miR210-3p stimulates endothelial progenitor cell angiogenesis and inhibits RGMA. When miR210-3p is overexpressed, EPC proliferation was greater than that of those who did not. In contrast, miR210-3p did no alter the mRNA level for RGMA in the mimics. Additionally, the luciferase-reporter assay revealed that miR210-3p targets RGMA directly.

The ligand-binding activity of miR210-3p was demonstrated, but miR210-3p also showed anti-inflammatory and tumor-related activities. The miR-210-3p antagonists were synthesized using RNA from wild-type and mutant SIN3A. To transfect cells, the pMIR-reporter-plasmids were used.

Knockdown miR-210-3p promotes apoptosis and inhibits lung cancer cell proliferation. SIN3A, a key regulator of cell proliferation, may be inhibited by miR-210-3p. This could regulate cell proliferation and apoptosis. Lung cancer patients may find it useful to knock down miR-210-3p. Further studies are needed in order to confirm the therapeutic value of miR210-3p against lung cancer.

In OGD-treated EPCs, miR210-3p has been shown in vitro to increase angiogenesis and protect EPCs against hypoxia. These effects may partially be due to the suppression of RGMA. Further research is needed to determine if miR210-3p suppresses downstream signals in EPCs. The findings could provide a theoretical basis to stroke treatment and may suggest a new therapeutic approach.

SIN3A is directly targeted, but miR210-3p also influences TWIST1, which is essential for cell proliferation. It also regulates migration and apoptosis. It may be a potential therapeutic target of NSCLC. If further studies are conducted, it could be used to treat NSCLC.

Several studies have shown that miR-210-3p expression and serum levels of SIN3A can serve as diagnostic and prognostic markers in NSCLC. These studies have focused mainly on miR210's prognostic power, with some promising results. Further studies are necessary to determine whether miR-210 affects other cancer markers. What is the role of miR210 in cancer?

Inhibition of miR-210-3p suppresses lung cancer cell viability, migration, and invasion. Inhibition of miR-210-3p also inhibits the expression of the anti-apoptotic protein Bcl-2. The findings suggest that miR-210-3p could be a potential therapeutic target for lung adenocarcinoma. The next step in this process is to study the role miR210-3p for lung cancer.

SIN3A decreased in invasiveness in A549 cells after it was downregulated

MiR210 regulates proliferation, apoptosis and survival of human U251 cells. This is done by downregulating SIN3A expression. A novel therapeutic strategy for glioma may be to downregulate SIN3A. However, this study has some limitations. The results of this study need further studies. This study shows that miR210 may also regulate SIN3A expression.

It is not clear what role SIN3A plays in tumor growth or invasion. This gene is involved in the regulation of the transcription of several genes, including those that regulate transcription. It binds to DNA binding proteins and transcriptional activater CBP. SIN3A binds with promoter regions of the nucleus and regulates expression of CDKN2A.

Cell apoptosis can be measured by using transfected or untransfected A549 cell lines. The cells from both groups spread to bottom of dish, while the transfected cells spread to the bottom. Bromodeoxyuridine was also added before 3 h to the culture medium to detect apoptosis.

Both SIN3A (and SIN3B) play important roles during normal development, as well as in breast cancer prevention. SIN3A & SIN3B are encoded in mammalian cells by two distinct genes. These proteins play different roles in many developmental processes. Knockdown of SIN3B decreased A549 cell transwell invasion through Matrigel while downregulation of SIN3A increased A549 cells' ability to invade 3D extracellular matrix.

MiR-124, a small molecule that has potential therapeutic effects for gastric cancer, is available. Downregulation of SIN3A inhibits the expression of several tumor suppressor genes and increases the invasive behavior of A549 cells. Furthermore, miR-124 targets rho-associated protein kinase 1 and inhibits the growth of gastric cancer cells. The results of this research suggest that miR124 could be a viable treatment strategy for gastric carcinoma. It also targets RPIA mRNAs iASPP.

SIN3A downregulation led to a decrease in Mxd1, which is a repressive protein complex that is essential for malignant melanomas. Downregulation of SIN3A also increased Mxd1 and its interaction with Max. MiR-202 also suppressed the proliferation of A549 cells. MiR202 also inhibits miR201.