|Immunogen:||Recombinant protein of human SOX2|
Western Blot: 1:500- 1:1000
Embryonic stem cells are derived from the inner cell mass of the blastocyst and are unique in their pluripotent capacity and potential for self-renewal. Sox2 is one of a set of transcription factors that are crucial for the maintenance of pluripotency (1). Sox2, Oct-4, and Nanog cooperate in this network (1-3), and siRNA knockdown of either Sox2 or Oct-4 results in loss of pluripotency (4,5). Chromatin immunoprecipitation experiments have shown that Sox2 and Oct-4 bind to thousands of gene regulatory sites, highlighting the importance of these transcription factors in early embryonic development (6,7). It has recently been shown that Sox2 is amplified in lung and esophageal squamous cell tumors (8).
|Buffer:||PBS with 0.02% sodium azide, 50% glycerol, pH7.3.|
|Storage:||Store at -20℃. Avoid freeze / thaw cycles.|
1. SOX2 Immunohistochemistry Frozen Tissues dilution 1:100 on cortex tissues of wild type mouse “enlargement 40x 03”
2. SOX2 Immunohistochemistry Frozen Tissues dilution: 1:100 on striated tissues of wild type mouse “enlargement 63x”
3. Western blot analysis of brain cell lysate using SOX2 antibody.
4. Immunohistochemistry of paraffin-embedded rat brain using SOX2 antibody at dilution of 1:100 (400x lens).
5. Immunohistochemistry of paraffin-embedded mouse brain using SOX2 antibody at dilution of 1:100 (400x lens).
6. Immunofluorescence analysis of MCF7 cell using SOX2 antibody. Blue: DAPI for nuclear staining.
References for SOX2 Polyclonal Antibody (AB-83387)
Application: WB, IF
Title: NSPc1 promotes cancer stem cell self-renewal by repressing the synthesis of all-trans retinoic acid via targeting RDH16 in malignant glioma
Journal: Cell death and disease
Application: IP , IF:
Title: FOXM1 contributes to taxane resistance by regulating UHRF1-controlled cancer cell stemness
Journal: Cell death & disease
Title: Acidosis enhances the self-renewal and mitochondrial respiration of stem cell-like glioma cells through CYP24A1-mediated reduction of vitamin D.