Snip1 Antibodies

Smad nuclear-interacting protein 1 (Snip1)

Down-regulates NF-kappa-B signaling by competing with RELA for CREBBP/EP300 binding.

Involved in the microRNA (miRNA) biogenesis.

biogenesis. Might be involved in cyclin-D1/CCND1 mRNA stability through the SNARP complex which partners with both the 3'end of the CCND1 gene and its mRNA (By similarity).

Gene Information

Mouse
Gene Name:	Snip1
Uniprot:	Q8BIZ6
Entrez:	76793

Family

Belongs to:
No superfamily

Alternative Names

dJ423B22.2; FHA domain-containing protein SNIP1; FLJ12553; RP3-423B22.3; Smad nuclear interacting protein (SNIP1); Smad nuclear interacting protein 1; smad nuclear-interacting protein 1

Molecular Weight

Mass (kDA):
44.415 kDA

Genomic Context

Mouse
Location:	4|4 D2.2
Sequence:	4;

Diseases

• Malignant Neoplasms
• Neoplasms
• Cell Transformation, Neoplastic
• Osteosarcoma
• Fibrosis
• Malignant Squamous Cell Neoplasm
• Tongue Neoplasms
• Cicatrix
• Non-small Cell Lung Carcinoma
• Bone Neoplasms
• Hypoxia
• Malignant Neoplasm Of Lung

• Cicatrix, Hypertrophic
• Carcinoma
• Carcinogenesis
• Tongue Squamous Cell Carcinoma
• Epilepsy
• Usher Syndrome
• Retinoblastoma

Pathways

• Cell Proliferation
• Cell Cycle
• Rna Processing
• Localization
• Aging
• G1 Phase
• Cell Growth

• Mesoderm Formation
• Epithelial To Mesenchymal Transition

PTMs

• Phosphorylation

• Nitration

• Ubiquitination

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Snip1

Best Uses Of The SNIP1 Marker

You've likely heard of the SNIP1 Marker, but are unsure of its use? Read on to learn more about its functions, overexpression, and knockdown. Afterwards, you'll have the knowledge to successfully use it for your research. The SNIP1 marker is a specific AFAP1-AS1 homology-based polypeptide that allows you to easily and quickly visualize this gene.

SNIP1 Marker

The SNIP1 marker is an important biomarker for cervical cancer research. Its expression is regulated by miRNA and SNIP. This study highlights the novel regulatory link between SNIP and miR29a, which plays a master regulator role in controlling cell proliferation and migration. The manuscript is well-written and easy to understand. It gives sufficient background on miRNA. Although the authors' discussion should include more details on the role of miR29a, it is easy to see that the study is generally well-planned.

SNIP1 is a nuclear protein that contains the Forkhead-associated domain and a nuclear localization signal. SNIP1 interacts with Smad proteins through its carboxyl terminus and its amino terminus harbors binding sites for Smad1 and Smad2, and the coactivator CBP/p300. SNIP1 inhibits TGF-b signaling in p300-dependent reporter constructs.

GST fusion proteins expressing SNIP1 were produced and purified using glutathione beads. Using a full-length Smad1 gene as bait, the fusion protein B42-SNIP1 was transformed into the yeast strain EGY48. The yeast strain also contained a transfected LexAop-Leu-2 reporter and the ura-3 selective marker. Transformants were selected using U-W and U-H-W plates.

Moreover, the SNIP1 molecule is a dual role regulator of gene expression. Its relative contribution may differ depending on the context and gene. However, it is important to note that SNIP1 may regulate ATR-dependent DNA damage responses. Its cellular function may influence the response to these insults. The role of SNIP1 in the immune system is one of the most intriguing questions for researchers.

Interestingly, GST-SNIP1 lacks the NLS, which may affect the protein's ability to interact with Smad4. Since the SAD domain is constitutively nuclear, it may prevent SNIP1 from binding to it. However, GST-SNIP1-215 lacks the NLS, which may be the culprit in restricting its interaction with SNIP1.

A recent study showed that the SNIP1 protein is expressed at a significantly higher level in UC and CD than in healthy control cells. However, the data were representative of three independent experiments. Its protein levels were analyzed using glutathione agarose and SDS-PAGE. The data were expressed as mean + SEM. A similar analysis was performed for a control group.

AFAP1-AS1

The AFAP1-AS1 Marker is a potential target for lung cancer therapy. It promotes lung cancer cell migration and invasion by mediating the binding of SNIP1 to c-Myc. Here we report on a study using in situ hybridization to examine the AFAP1-AS1 marker in lung cancer tissues and normal lung epithelial cells.

The AFAP1-AS1 gene is upregulated in both HuCCT1 tumors and adjacent normal tissues. Knockdown of AFAP1-AS1 inhibited HuCCT1 cell proliferation, metastasis, and TFK-1 expression in tumors. Earlier studies suggested that this gene may play an oncogenic role in CCA pathology. Currently, the AFAP1-AS1 gene is an active target in clinical trials.

AFAP1-AS1 is a long non-coding RNA that is overexpressed in several cancer types. The aim of this study was to identify its role in lung cancer by investigating AFAP1-AS1 expression in paraffin-embedded tumors. In addition, the researchers looked at the expression of AFAP1-AS1 and its association with lung tumors, TNM stages, and poor patient survival.

The AFAP1-AS1 marker in Boster Bio was validated by quantitative RT-PCR in NSCLC tissues using an in-house qRT-PCR. A positive qRT-PCR resulted in a positive response for the AFAP1-AS1 gene in each of the tissues tested. In addition, the AFAP1-AS1 gene was also found to be associated with a variety of cancer genes and protein levels in the NSCLC patient profile.

AFAP1-AS1 is expressed in the nucleus and plays an oncogenic role in OS tumorigenesis. AFAP1-AS1 is expressed at higher levels in the nucleus than in the cytosol, thereby enhancing the likelihood of cancer in OS-related tumorigenesis. The expression of AFAP1-AS1 was reduced after knockdown of the gene in BSG-cells.

Knockdown of AFAP1-AS1 inhibits EMT and reduces the expression of Twsit1. The knockdown of SNIP1 also prevented c-Myc transcription in these cells. These studies demonstrate that the AFAP1-AS1 gene is a key target for the EMT-related transcription factor RhoC. So, AFAP1-AS1 is a valuable marker for OS research.

SNIP1 knockdown

The role of SNIP1 in the epithelial-mesenchymal transition is unclear. It is thought to be involved in the regulation of the GSK-3I2/Snail signaling pathway, which facilitates the process of epithelial-mesenchymal transition (EMT). In addition, SNIP1 inhibits the proliferation and metastasis of CCA cells. Thus, SNIP1 is an important therapeutic target.

SNIP1 overexpression

SNIP1 is a gene that promotes lung cancer cell migration and invasion. Its overexpression in lung cancer cells may be an attractive therapeutic target. In the present study, we used a human lung cancer cell line (A549) and a normal human lung epithelial cell line (PC9) to investigate its role in lung cancer. The researchers used Lipofectamine RNAiMAX reagent to transfect the cells with SNIP1-AS1 siRNA and a pool of siRNA1 and siRNA2.

SNIP1 acts on c-Myc degradation through binding to AFAP1-AS1. Inhibition of SNIP1 by AFAP1-AS1 abolishes this effect. However, the role of SNIP1 in c-Myc degradation is not fully understood. In a subsequent study, we identified a gene in the Boster Bio c-Myc promoter that regulates the expression of SNIP1.

In this study, we used A549 cells injected into the tail vein of mice. We then used qRT-PCR to assess the effects of AFAP1-AS1 overexpression on lung metastasis. In the presence of AFAP1-AS1, the number of lung metastases was significantly reduced in the knockdown group, while the SNIP1-AS1 overexpression group showed higher levels of metastatic nodules. We then calculated the total area of the metastatic nodules in both groups.

MiR-34 promotes differentiation and inhibits proliferation in myoblasts by targeting the YY1 transcription factor. This molecule has been found to be important in the development of skeletal muscle in cattle. When overexpressed in bovine myoblasts, it inhibits myogenesis and apoptosis, which may contribute to the suppression of myoblast proliferation and differentiation in bovine muscle cells.