basic FUNCTION
| core promoter element binding protein |
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acting as an inhibitor of cell proliferation by counteracting the function of the c-Jun proto-oncoprotein involving enhanced c-Jun degradation by the proteasome-dependent pathway, and further reinforces KLF6 as a potential tumor suppressor gene product |
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having a role as a multifunctional transcriptional regulator capable of mediating adipocyte differentiation through gene repression |
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involved in differentiation and development, growth-related signal transduction, cell proliferation, apoptosis, and angiogenesis |
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playing an important role in the development or progression of sporadic gastric cancers |
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inducing cell death by apoptosis via BCL2L1 induction and p53 repression |
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transcription factor involved in the regulation of ASAH1 gene expression |
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playing an important role of tumour suppressor gene in gastric cancer development and progression |
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tumor suppressor activity by down-regulating PTTG1 oncogene |
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KLF6 regulation of GCK contributes to the development of hepatic insulin resistance |
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is frequently inactivated in human cancer and has significant roles in cellular proliferation, apoptosis, differentiation and development |
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is a novel regulator of hepatic glucose and lipid metabolism in fatty liver |
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is a novel transcriptional regulator of macrophage polarization |
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having function in response to malignant transformation, suggesting the relevance of KLF6 in controlling cell proliferation and hindering tumorigenesis |
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is a relevant participant in cytotrophoblast fusion |
CELLULAR PROCESS
| cell life, differentiation
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| cell life, cell death/apoptosis
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nucleotide, transcription, regulation
|
text
| transcriptional activator, B cell differentiation |
small molecule
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metal binding,
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| Zn2+ |
protein
| regulation and maintenance of the basal expression of TATA box-less genes |
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binding to the GC rich binding sites of the HIV-1 promoter |
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repressor of the proto-oncogene Delta-like 1 (DLK1), a gene encoding a transmembrane protein that inhibits adipocyte differentiation |
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interaction with HDAC3 (potential mechanism underlying adipogenesis) |
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downregulates the alpha1-proteinase inhibitor gene in corneal epithelial cells and may thereby be involved in keratoconus |
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interacting with CDH1 (transcriptional target of the KLF6 tumor suppressor) |
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E2F1 and KLF6 show cooperation in activating the DAPK2 promoter |
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interacting with ATF3 (ATF3 is a key mediator of KLF6-induced apoptosis in prostate cancer cells) |
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interaction between the C-terminal domain of LCOR and the transcription factor KLF6, a putative tumor suppressor in prostate cancer |
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KLF6 could directly bind and repress PTTG1 expression (down-regulation of the oncogene PTTG1 via the KLF6 tumor suppressor during induction of myeloid differentiation) |
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essential co-activator of NFKB1, suggesting new insight into the molecular regulation of RELA-dependent gene expression |
Phosphorylated by
| GSK3B (GSK3B directly phosphorylates KLF6, which augments its induction of CDKN1A and resultant growth suppression) |
Other
| regulation of the gene transcription is under control of a TATA-box independent initiation mechanism together with an evolutionary conserved array of positive cis-acting elements |
Other morbid association(s)
|
Type | Gene Modification | Chromosome rearrangement | Protein expression | Protein Function
|
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tumoral
|  
| LOH
|  
|  
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in primary prostate and astrocytic glioma | tumoral
| somatic mutation
|  
|  
|  
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in nasopharyngeal carcinoma | tumoral
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| LOH
|  
|  
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in gastric cancer | constitutional
|  
|  
| --over
|  
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during hepatic fibrosis | tumoral
|  
|  
|  
| loss of function
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inactivated in solid tumors | tumoral
|  
| deletion
|  
|  
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in high grade astrocytomas in progression to glioblastoma multiform, ependymoma, prostate carcinoma, renal, anaplastic or atypical meningioma, primary sarcomas with metastases | tumoral
|  
| LOH
|  
|  
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represents a clinically-relevant biomarker predicting patient survival and tumor recurrence and that dysregulation of KLF6 function plays an important role in head and neck squamous cell carcinomaprogression | tumoral
|  
|  
| --over
|  
|
n breast cancer | |
Susceptibility
|
to hepatocellular carcinoma (minor role) |
Variant & Polymorphism
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| |
Candidate gene
Marker
Therapy target
|
System | Type | Disorder | Pubmed |
neurology | acquired | | |
manipulating KLF6 or multiple KLF genes may be a useful strategy to add to existing approaches to increase the intrinsic regenerative capacity of mature CNS neurons damaged by injury or disease | cancer | hemopathy | | |
drugs that increase the KLF6 inhibition of PTTG1 may have a therapeutic application in acute myeloid leukemia (AML) treatment strategies | cancer | digestive | stomach | |
downregulation of KLF6-SV1 by siRNA may offer a new potential gene therapy approach for gastric cancer |
| | | |
| in mice, an increased SV1/Klf6 ratio, generated either by increasing SV1, decreasing Klf6, or both, accelerates hepatic carcinogenesis |