SP1 (Phospho-Thr739) ELISA Kit

Name: SP1 (Phospho-Thr739) ELISA Kit
SKU: DEIA-XYA1665
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse; Rat

Intended Use

The SP1 (Phospho-Thr739) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor SP1 protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated SP1 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on SP1 phosphorylation.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 2 Plates
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-SP1 (Phospho-Thr739) Antibody (Rabbit Polyclonal): 60 μL (100x), Red
7. 100x Anti-SP1 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL (1x), Glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL (1x), Glass
11. Primary Antibody Diluent: 12 mL (1x), Clear
12. Ready-to-Use Substrate: 12 mL (1x), Brown
13. Stop Solution: 12 mL (1x), Clear
14. Crystal Violet Solution: 12 mL (1x), Glass
15. SDS Solution: 24 mL (1x), Clear
16. Adhesive Plate Seals: 4 Seals

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Sp1 in Astrocyte Is Important for Neurite Outgrowth and Synaptogenesis

MOLECULAR NEUROBIOLOGY

Authors: Hung, Chia-Yang; Hsu, Tsung-, I; Chuang, Jian-Ying; Su, Tsung-Ping; Chang, Wen-Chang; Hung, Jan-Jong

Abstract

In this study, we found that Sp1 was highly expressed in astrocytes, implying that Sp1 might be important for the function of astrocytes. Sp1/GFAP-Cre-ERT2 conditional knockout mice were constructed to study the role of Sp1 in astrocytes. Knockout of Sp1 in astrocytes altered astrocytic morphology and decreased GFAP expression in the cortex and hippocampus but did not affect cell viability. Loss of Sp1 in astrocytes decreased the number of neurons in the cortex and hippocampus. Conditioned medium from primary astrocytes with Sp1 knockout disrupted neuronal dendritic outgrowth and synapse formation, resulting in abnormal learning, memory, and motor behavior. Sp1 knockout in astrocytes altered gene expression, including decreasing the expression of Toll-like receptor 2 and Cfb and increasing the expression of C1q and C4Bp, thereby affecting neurite outgrowth and synapse formation, resulting in disordered neuron function. Studying these gene regulations might be beneficial to understanding neuronal development and brain injury prevention.

HPV8 activates cellular gene expression mainly through Sp1/3 binding sites

VIROLOGY

Authors: Kirschberg, Matthias; Heuser, Sandra; Syed, Adnan S.; Steger, Gertrud; Majewski, Slawomir; Hufbauer, Martin; Akguel, Baki

Abstract

The human papillomavirus type 8 (HPV8) is associated with skin cancer development. The goal of this study was to investigate the effects of HPV8 oncoproteins on cellular gene expression and the identification of key regulators. We performed affymetrix microarray analyses to identify differentially expressed genes and common sequence motifs and identified Sp1/3 binding sites as being crucial. In transient transfection assays, we confirmed that HPV8-E7 stimulates the activity of Sp1/3 promoters. Interestingly, the HPV8-E7(L23A) mutant, which cannot trigger keratinocyte invasion was unable to activate fibronectin gene expression. In skin models or HPV8 positive skin cancers we found a peculiar deposition of fibronectin in the dermal compartment, and a correlation of Sp3 and fibronectin in the nucleus of HPV8-positive keratinocytes. Taken together, we identified that HPV8-E7 exerts control over cellular gene expression through Sp1/3 binding motifs, which may contribute to HPV8-mediated keratinocyte transformation and subsequent fibronectin-dependent invasion.