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KLF8 encodes a protein which is a member of the Sp/KLF family of transcription factors. Additionally we are shipping KLF8 Antibodies (51) and many more products for this protein.
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Results demonstrate a novel role of Klf8, achieved via modulation of p53 (show TP53 Proteins) and met expression, in the maintenance neuronal progenitors and development of Purkinje cells and the proliferation of granule cells in the cerebella of zebrafish embryos
Overexpression of KLF8 may contribute to the progression of pancreatic cancer, and downregulation of KLF8 expression by lentivirus-delivered shRNA is a novel therapeutic approach for PC.
KLF8 plays a crucial role in proliferation and migration of bladder cancer cells
KLF8-induced FHL2 (show FHL2 Proteins) activation is a novel and critical signaling mechanism underlying human colorectal cancer invasion and metastasis.
KLF8 and miR141/EGFR (show EGFR Proteins) have roles in signaling pathway potentially crucial for breast cancer malignancy
KLF8 suppression induced cell differentiation and inhibited tumorigenesis in colorectal cancer
MiR (show MLXIP Proteins)-135a inhibits migration and invasion and regulates epithelial-mesenchymal transition-related marker genes by targeting KLF8 in lung cancer cells.
KLF8 is a novel epithelial to mesenchymal transition regulating transcription factor that involved in the progression of gastric cancer.
In this review, we focus on the functions, roles, and regulatory networks of these five KLFs in HCC (show FAM126A Proteins), summarize key pathways, and propose areas for further investigation
A novel KLF8 to EPSTI1 to VCP (show vcp Proteins) to NF-kappaB (show NFKB1 Proteins) signaling mechanism potentially critical for breast cancer invasion and metastasis.
KLF8 is involved in hypoxia-induced multidrug resistance through inhibiting apoptosis and increasing the drug release rate by directly regulating MDR1 transcription.
Klf8 is highly expressed in various regions of the mouse brain and in particular in the neurons, where it was localized in the cell nuclei.
KLF3 and KLF8 have overlapping roles in vivo and participate in the silencing of embryonic globin expression during development.
KLF8 is a key component of the transcription factor network that controls terminal differentiation during adipogenesis.
PARP-1 (show PARP1 Proteins) as a novel KLF8-binding and -regulating protein and provided new insights into the mechanisms underlying the regulation of KLF8 nuclear localization, stability, and functions.
These results identified the KLF8 activation domain located between residues 101-260 where the well-conserved Q118 and Q248 are essential for recruiting p300 (show NOTCH1 Proteins) and PCAF (show KAT2B Proteins) to activate target gene transcription.
sumoylation of KLF8 negatively regulates its transcriptional activity and cellular functions
Klf8 is repressed by Klf3 (show KLF3 Proteins) and activated by Klf1 (show KLF1 Proteins) in vivo.
KLF8 has two N terminal regulatory regions, one surrounding S165 and K171 and the other being two tandem ZFs, which are critical for the regulation of KLF8 nuclear localization and its cellular functions
results demonstrate that KLF8 can participate in regulating expression of alternate forms of HuR (show ELAVL1 Proteins) mRNA along with NF-kappaB (show NFKB1 Proteins) and other factors, depending on cellular contexts
This gene encodes a protein which is a member of the Sp/KLF family of transcription factors. Members of this family contain a C-terminal DNA-binding domain with three Kruppel-like zinc fingers. The encoded protein is thought to play an important role in the regulation of epithelial to mesenchymal transition, a process which occurs normally during development but also during metastasis. A pseudogene has been identified on chromosome 16. Alternative splicing results in multiple transcript variants.
Krueppel-like factor 8
, kruppel-like factor 8
, Kruppel-like factor 8
, basic krueppel-like factor 3
, basic kruppel-like factor 3
, zinc finger protein 741
, Kruppel-like factor 8, pseudogene 1