SMAD6 Antibodies

Mothers against decapentaplegic homolog 6 (SMAD6)

Acts as a mediator of TGF-beta and BMP antiflammatory activity.

Suppresses IL1R-TLR signaling through its direct interaction with PEL1, preventing NF-kappa-B activation, nuclear transport and NF-kappa-B-mediated expression of proinflammatory genes.

May block the BMP-SMAD1 signaling pathway by competing with SMAD4 for receptor-activated SMAD1-binding. Binds to regulatory elements in target promoter regions.

Gene Information

Human
Gene Name:	SMAD6
Uniprot:	O43541
Entrez:	4091

Family

Belongs to:
dwarfin/SMAD family

Alternative Names

hSMAD6; HsT17432; MAD homolog 6; MADH6SMAD, mothers against DPP homolog 6 (Drosophila); MADH7; mothers against decapentaplegic homolog 6; Mothers against decapentaplegic, drosophila, homolog of, 6; Mothers against DPP homolog 6; SMAD 6; SMAD family member 6MAD, mothers against decapentaplegic homolog 6 (Drosophila); SMAD, mothers against DPP homolog 6; Smad6

Molecular Weight

Mass (kDA):
53.497 kDA

Genomic Context

Human
Location:	15q22.31
Sequence:	15; NC_000015.10 (66702110..66782849)

Tissue Specificity

Ubiquitous in various organs, with higher levels in lung. Isoform B is up-regulated in diseased heart tissue.

Subcellular Localizations

Nucleus.

Diseases

• Malignant Neoplasms
• Neoplasms
• Carcinoma
• Fibrosis
• Malignant Paraganglionic Neoplasm
• Cell Transformation, Neoplastic
• Hypertrophy
• Inflammation
• Kidney Diseases
• Tissue Adhesions
• Pancreatic Neoplasm
• Carcinogenesis
• Nervousness

• Hypertensive Disease
• Growth Arrest
• Pulmonary Hypertension
• Adenocarcinoma
• Malignant Squamous Cell Neoplasm
• Idiopathic Pulmonary Hypertension
• Lung Diseases

Interacting Proteins

• PRKX
• RUNX2
• SMAD1
• STAMBP

Pathways

• Cell Proliferation
• Pathogenesis
• Cell Growth
• Cell Differentiation
• Localization
• Rna Interference
• Secretion
• Osteoblast Differentiation
• Cell Cycle
• Chondrocyte Differentiation
• Ossification
• Gastrulation
• Bmp Signaling Pathway

• Translation
• Cartilage Development
• Cell Death
• Chondrocyte Proliferation
• Angiogenesis
• Endochondral Ossification
• Regeneration

PTMs

• Phosphorylation
• Ubiquitination
• Methylation
• Demethylation
• Cleavage

• Acetylation
• Sumoylation
• Gamma-carboxylation
• Dephosphorylation
• Geranylgeranylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SMAD6

Best Uses Of The SMAD6 Marker For Glioma

In this article, we will discuss the use of the SMAD6 marker as a prognostic marker for glioma. This enzyme plays a role in the negative regulation of TGF-beta/activin signaling. It also interacts with Hox family transcription factors. Finally, we will discuss its targets, miR-330-5p and miR-326.

SMAD6 is a prognostic marker for glioma

There is a growing body of evidence that SMAD6 is an important biomarker in gliomas. While the results of this study are preliminary, these findings suggest that the protein may be a valuable tool for glioma diagnosis and treatment. Moreover, it may also serve as a therapeutic target for glioma. To date, however, only a few studies have looked at SMAD6.

The researchers found that the expression of SMAD6 was significantly correlated with NF-kB activity and down-regulated in 15 different glioma cell lines. Furthermore, the expression of p-Smad2 was significantly associated with shorter survival in patients with glioma. This finding could pave the way for more accurate diagnosis and treatment for patients with glioma.

The researchers also conducted IHC analysis on 161 glioma tissue sections. They scored these tumor sections by two independent observers. In addition, they categorized the staining intensity into light yellow, moderate yellow, and brown. The resulting index was then calculated. Moreover, the researchers noted that the presence of SMAD6 in tumors is associated with poor prognosis, as it is the most common form of glioma.

Another study involving a small number of patients found that SMAD6 was a valuable prognostic marker for gliomas. Its expression is associated with poor prognosis in patients with high-grade glioma, and inhibiting EGFR may be an important therapeutic target for the disease. However, further studies are needed to confirm these findings and identify whether or not SMAD6 is a viable prognostic biomarker in glioma.

It functions in the negative regulation of BMP and TGF-beta/activin-signalling

This article will discuss the role of Smad in the regulation of bone remodeling, osteoporosis, and bone formation. The Smad signaling pathway is essential for maintaining bone homeostasis by regulating the differentiation of osteoblasts and osteoclasts. Smad signalling has important roles in bone formation and homeostasis, and inhibiting this pathway may be an effective osteoporosis treatment.

The SMAD6 gene is located on the chromosomes. The SMAD6 gene contains two copies, one for each protein. The SMAD2 and Smad6 genes are highly conserved. SMAD6 interacts with other proteins and with other genes in order to activate the corresponding signaling pathways.

Smad3 and Smad2 overexpression stimulated cell proliferation but repressed lipid accumulation. In the absence of TGF-b, the Smad3 and Smad2 mutants increased cell growth by threefold or more. However, Smad3DSSVS inhibited growth by 30% compared to the vector alone.

Both Smad1 and Smad3 are critical for osteogenesis and maintain bone structure. By blocking or suppressing these pathways, Smad1 and Smad2 play critical roles in bone formation. Further studies are needed to determine which of these proteins can function independently or synergistically. They also regulate the expression of Smad5 and Smad6 mRNA.

SMAD7 overexpression in pancreas and human lung cancers promotes the development of liver metastases. In addition, Smad7 overexpression in mice results in severe colitis. Antisense oligonucleotide inhibits this inflammation and reverses its malignant transformation. The overexpression of Smad7 is associated with genetic polymorphisms in Smad7.

SMAD6 and Smad7 function as negative regulators of adipogenesis. Moreover, they suppress adipocyte differentiation by inhibiting TGF-b responses and augment the effect of TGF-b on adipocyte differentiation. These findings support the role of Smads in normal adipocyte differentiation.

SMAD7 and SMAD6 are two inhibitory SMADs, which may play a crucial role in intracellular signaling. Inhibition of Smad6 may enhance the transcriptional response to TGF-b by inhibiting Smad3 and Smad4 in mesangial cells. Likewise, increased Smad7 and Smad6 expression may have a role in TGF-b/Smad signaling.

It interacts with Hox family transcription factors

The homeodomain transcription factor SMAD6 interacts with members of the Hox family to regulate many pathways during development. These proteins recognise similar sequences in vitro and in vivo and have remarkably diverse functions. Their specificity is acquired through cooperative binding with cofactors. Although there are few known direct targets, these factors participate in a broad range of cellular functions. This article reviews recent research to understand how SMAD6 interacts with Hox family transcription factors.

The SMAD6 protein regulates the expression of a number of Hox genes, including those encoding the cofactors Bgf2. In addition to regulating Hox gene expression, SMAD6 also controls the expression of several genes containing Hox proteins. During embryonic development, HOXB7 acts as a direct target of the basic fibroblast growth factor (Bfgf), a factor involved in controlling segment formation. Hox proteins also control the expression of several molecules, including the TALE transcription factor, which controls the expression of HOX genes.

The Hox genes were first identified as regulators of anterior-posterior pattern formation during embryonic development. They have since been discovered to be active in normal adult cells. The Hox proteins are believed to function as master genes in cellular identity, and to regulate a broad range of genes involved in cell division, adhesion, migration, morphological differentiation, and apoptosis.

The isolated C-terminal domain of mammalian Smad6 inhibits BMP signaling in Xenopus embryos. These species-specific sequence differences make it impossible for the hypothetical binding protein to recognize a homologous protein from another species. These results suggest that the Smad6 N and DN proteins are not functionally equivalent. Smad6 N and DN do not interact with each other in vitro.

The mRNA for the Smad6 gene was isolated from the RNA of Smad6-deficient chondrocytes at E15.0 and expressed in their cytoplasm and nucleus. At P0 and P1, the expression of Smad6 was higher in the upper hypertrophic zones and decreased in terminal hypertrophic chondrocytes. In addition, Smad6-deficient chondrocytes had increased levels of collagen production, suggesting that Smad6 is a direct regulator of hypertrophic differentiation and chondrogenesis.

It is a target of miR-330-5p and miR-326

The hsa_circ_0000517 gene is an SMAD6 target. It is involved in the regulation of signal transduction and cell proliferation. The miR-330-5p and miR-326 target genes are highly expressed in the human tumor microenvironment. However, the molecular mechanisms of these two microRNAs remain unclear. To further investigate their relationship, the researchers used the RIP assay. They also used the RIP assay to determine whether miR-330-5p and miR-326 inhibited SMAD6.

In HCC, miR-326 suppresses protein levels of MMP2 and Cyclin D1. The miR-326 mimics restored these effects by increasing SMAD6 levels. Inhibitors of miR-326 partially restored the effects of miR-326. The miR-330-5p and miR-326 mimics suppressed the expression of SMAD6 and restored its inhibitory effects.

Using the RIP assay, the researchers identified the SMAD6 as a target of miR-330-5 and miR-326. SMAD6 and miR-330-5p have the same function in the cancer cell lineage. They target different pathways, so identifying the specific targets of these two miRNAs may be useful in developing new therapeutics.

SMAD6 is an important feedback suppressor of BMP/SMAD signaling. An imbalance of BMP signaling can accelerate the progression of cancers. During BMP-mediated invasion, SMAD6 influences the behavior of breast cancer cells. It also inhibits PIAS3-mediated suppression in glioma cells. Furthermore, BRG1 stimulates the expression of SMAD6 in HCC cells.

MiR-330-5p and miR-327 target SMAD6 in HCC tissues. The SMAD6 target hsa_circ_0000517, the HSC marker of hsa_circ_0000516, was revealed in the same experiments. Further studies are necessary to determine the exact role of SMAD6 in the pathogenesis of cancer cells.

The mRNA-miRNA-lncRNA-circRNA network generated from the COAD metastasis mRNAs and lncRNAs. To determine the RNA hubs, the expression levels of mRNAs within the network were calculated. Using survival analysis, mRNAs and miRNAs that were identified as significant by miRNAs were selected and analyzed for their functions. The functional roles of these miRNAs were also analyzed using previously published data.

To understand the role of these microRNAs, researchers must identify the genes associated with psoriasis. The regulatory network of these microRNAs is defined by five different types of transcriptional interactions. These relationships can be categorized by gene, protein family, molecular function, and biological process. The gene-miRNA-gene relationship, as well as the microRNA-transcription factor relationship, can be identified by this method.