Immunofluorescent analysis of Lin28 (green) showing cytoplasmic staining of NCCIT cells (right panel) compared to HeLa cells (left panel). The cells were fixed with formalin for 15 minutes, permeabilized with 0.1% Triton X-100 in TBS, washed, and then blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were probed with a DyLight 488-conjugated Lin28 monoclonal antibody (Product # MA1-016-D488) in 3% BSA-PBS at a dilution of 1:100 and incubated for 1 hour at 37C in the dark. F-Actin (both panels, red) was stained with DyLight 554 Phalloidin (Product # 21834) and nuclei (both panels, blue) were stained with DAPI. Images were taken at 60X magnification.
|Tested species reactivity||Human, Mouse|
|Host / Isotype||Mouse / IgG|
|Immunogen||Full-length human recombinant protein expressed in bacteria|
|Storage buffer||PBS with proprietary stabilizer|
|Contains||0.02% sodium azide|
|Storage Conditions||4° C, do not freeze|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||1:50-1:500|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
MA1-016-D488 has been successfully used in ICC/IF and flow cytometry applications on human and mouse samples.
MA1-016-D488 can be used for immunofluorescence analysis of LIN28 in human iPSCs.
LIN28A/B are expressed in various cancers and ES cells. LIN28 is a cytoplasmic protein, that acts as a 'translational enhancer', driving specific mRNAs to polysomes and thus increasing the efficiency of protein synthesis. LIN28 is a negative regulator of microRNA (miRNA) biogenesis by specifically binding the precursor of let-7 (pre-let-7). Let-7 miRNAs have been implicated in repression of oncogenes such as ras and myc. LIN28 expression decreases during differentiation of ES cells or upon induction of neuronal differentiation by retinoic acid.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.