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Data show that forced expression of Kruppel-like factor 9 (Klf9) in the brain of thyroid-intact tadpoles increased baseline thyroid hormone receptor-beta (trb (show THRB Proteins)) mRNA and enhanced trb autoinduction.
Induced expression of BTEB1 in XTC-2 cells caused accelerated and enhanced autoinduction of the TrbetaA gene.
The expression of KLF9 is down-regulated in esophageal squamous cell carcinoma and inversely correlated with the clinical features.
Suggest role for miR (show MLXIP Proteins)-570/KLF9 molecular network in controlling lung carcinoma progression.
TRs cooperate with KLF9 to regulate hepatocyte proliferation and differentiation and early stages of organogenesis and that TRs exert widespread and important influences on ESC biology.
Myometrial KLF9 may contribute to the onset of human parturition through its regulation of PGR (show PGR Proteins) expression and inflammatory signaling networks.
the expression of KLF9 is up-regulated in human ovarian cancer; KLF9 knockdown significantly inhibited cell proliferation and resulted in cell cycle arrest in the G0/G1 phase
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
Palmitic acid increases Ppargamma (show PPARG Proteins) and Klf6 (show KLF6 Proteins) & Klf9 gene expression and promotes triglyceride accumulation in HepG2 cells.
Reduced KLF9 expression is associated with glioma.
Data indicate that integrin alpha6 repression by Kruppel-like factor-9 (KLF9) inhibits glioblastoma cell stemness and tumorigenicity.
increased KLF9 expression is in part responsible for CYP2D6 (show CYP2D6 Proteins) induction during pregnancy via the potentiation of HNF4alpha (show HNF4A Proteins) transactivation of CYP2D6 (show CYP2D6 Proteins).
Study identified genomic targets of Klf9 in hippocampal neurons which raise some indication about it functions in chromatin, and neuronal morphology regulation and survival across the lifespan.
Kruppel-like factor 9 (KLF9) is a haploinsufficient tumor suppressor in the ApcMin/+ mouse colon by suppressing expression of ISG15 (show ISG15 Proteins), an apoptosis-inhibiting cytokine.
in endometrial stromal cells, KLF9 provides coincident regulation of Notch (show NOTCH1 Proteins), Hh, and steroid receptor (show ESR2 Proteins) signaling pathways, which when deregulated, underlie establishment and/or progression of endometriosis
Nrf2 (show NFE2L2 Proteins) amplifies oxidative stress via induction of Klf9.
KLF9 bound the KLF binding element at position -874 of the mouse C/EBPbeta (show CEBPB Proteins) promoter.
Klf9 is essential for turning off programmed cell death of Purkinje cells in organotypic cultures.
We showed that Kruppel-like factor 9 was a key mediator of this effect of T(3); the sudden physiological increase in T(3) during development is involved in the onset of the loss of axon regenerative capacity in purkinje cells.
KLF9 is an integral component of the T3-driven signaling cascade that promotes myelin regeneration.
Common variants at CDKAL1 (show CDKAL1 Proteins) and KLF9 are associated with body mass index in east Asian populations.
The protein encoded by this gene is a transcription factor that binds to GC box elements located in the promoter. Binding of the encoded protein to a single GC box inhibits mRNA expression while binding to tandemly repeated GC box elements activates transcription.
Kruppel-like factor 9
, gene 1
, gene 3
, basic transcription element binding protein 1 (gene 1)
, BTE-binding protein 1
, GC-box-binding protein 1
, Krueppel-like factor 9
, basic transcription element binding protein 1
, basic transcription element-binding protein 1
, transcription factor BTEB1
, BTEB transcription factor