Ignet

Gene Information

Gene symbol: TFPI

Gene name: tissue factor pathway inhibitor (lipoprotein-associated coagulation inhibitor)

HGNC ID: 11760

Synonyms: EPI, TFI, TFPI1

Related Genes

#	Gene Symbol	Number of hits
1	ABCB1	1 hits
2	ABCG2	1 hits
3	CD4	1 hits
4	CD8A	1 hits
5	CTBS	1 hits
6	CTCFL	1 hits
7	DNAJC5	1 hits
8	F2	1 hits
9	FLNA	1 hits
10	HDAC2	1 hits
11	MYC	1 hits
12	SETD2	1 hits
13	SFTPA1B	1 hits
14	SRC	1 hits

Related Sentences

#	PMID	Sentence
1	7775876	In 1991, the CSP/EPI developed a national plan to introduce national immunization of infants against hepatitis B in an attempt to control the magnitude and seriousness of the damage which viral hepatitis causes in terms of morbidity, mortality and serious sequelae as hepatitis B is an endemic disease in Egypt causing an important public health problem which requires urgent control.
2	11689645	In an in vitro cell depletion experiment, we demonstrated that the CTL activity against HBsAg elicited by EPI was attributed to CD8(+), not CD4(+), T cells.
3	12034092	When administered by EPI, CTB, LTR72 and LTK63 significantly augmented antibody responses to the influenza vaccine and protection against a lethal challenge in a mouse model.
4	18940220	Overall, there was a gross difference in the prevalence of anti-HBs marker between the EPI and OPD groups.
5	20605977	All RASV strains expressing PspA generated high antilipopolysaccharide antibody titers, indicating that expression of lacI did not interfere with the capacity to induce an immune response.
6	24489651	Elevated TFPI1 in DOX resistant cells was active, as thrombin protein levels were coincidentally low.
7	24489651	We observed elevated HIF1α protein in DOX resistant cells, and in cells with forced expression of TFPI1, suggesting TFPI1 induces HIF1α.
8	24489651	TFPI1 also induced c-MYC, c-SRC, and HDAC2 protein, as well as DOX resistance in parental cells.
9	24489651	Growth of cells in 1% O2 induced elevated HIF1α, BCRP and MDR-1 protein, and these cells were resistant to DOX.
10	24489651	Our in vitro results were consistent with in vivo patient datasets, as tumors harboring increased BCRP and MDR-1 expression also had increased TFPI1 expression.
11	24489651	Elevated TFPI1 in DOX resistant cells was active, as thrombin protein levels were coincidentally low.
12	24489651	We observed elevated HIF1α protein in DOX resistant cells, and in cells with forced expression of TFPI1, suggesting TFPI1 induces HIF1α.
13	24489651	TFPI1 also induced c-MYC, c-SRC, and HDAC2 protein, as well as DOX resistance in parental cells.
14	24489651	Growth of cells in 1% O2 induced elevated HIF1α, BCRP and MDR-1 protein, and these cells were resistant to DOX.
15	24489651	Our in vitro results were consistent with in vivo patient datasets, as tumors harboring increased BCRP and MDR-1 expression also had increased TFPI1 expression.
16	24489651	Elevated TFPI1 in DOX resistant cells was active, as thrombin protein levels were coincidentally low.
17	24489651	We observed elevated HIF1α protein in DOX resistant cells, and in cells with forced expression of TFPI1, suggesting TFPI1 induces HIF1α.
18	24489651	TFPI1 also induced c-MYC, c-SRC, and HDAC2 protein, as well as DOX resistance in parental cells.
19	24489651	Growth of cells in 1% O2 induced elevated HIF1α, BCRP and MDR-1 protein, and these cells were resistant to DOX.
20	24489651	Our in vitro results were consistent with in vivo patient datasets, as tumors harboring increased BCRP and MDR-1 expression also had increased TFPI1 expression.
21	24489651	Elevated TFPI1 in DOX resistant cells was active, as thrombin protein levels were coincidentally low.
22	24489651	We observed elevated HIF1α protein in DOX resistant cells, and in cells with forced expression of TFPI1, suggesting TFPI1 induces HIF1α.
23	24489651	TFPI1 also induced c-MYC, c-SRC, and HDAC2 protein, as well as DOX resistance in parental cells.
24	24489651	Growth of cells in 1% O2 induced elevated HIF1α, BCRP and MDR-1 protein, and these cells were resistant to DOX.
25	24489651	Our in vitro results were consistent with in vivo patient datasets, as tumors harboring increased BCRP and MDR-1 expression also had increased TFPI1 expression.
26	24658009	Hypomethylation of the CTCFL/BORIS promoter and aberrant expression during endometrial cancer progression suggests a role as an Epi-driver gene.
27	24658009	We investigated a unique collection of endometrial cancer precursor samples and clinically annotated primary and metastatic lesions for two evolutionary and functionally related transcription factors, CCCTC-binding factor (zinc finger protein) (CTCF) and its paralogue CTCF-like factor, also denoted Brother of the Regulator of Imprinted Sites (CTCFL/BORIS).
28	24658009	CTCF, a chromatin modeling- and transcription factor, is normally expressed in a ubiquitous fashion, while CTCFL/BORIS is restricted to the testis.
29	24658009	In cancer, CTCF is thought to be a tumor suppressor, while CTCFL/BORIS has been suggested as an oncogene.
30	24658009	Thus, CTCF and CTCFL/BORIS are found to diverge in the different subtypes of endometrial cancer, with CTCFL/BORIS activation through demethylation from precursors to metastatic lesions.
31	24658009	We thus propose, CTCFL/BORIS as an Epi-driver gene in endometrial cancer, suggesting a potential for future vaccine development.
32	24658009	Hypomethylation of the CTCFL/BORIS promoter and aberrant expression during endometrial cancer progression suggests a role as an Epi-driver gene.
33	24658009	We investigated a unique collection of endometrial cancer precursor samples and clinically annotated primary and metastatic lesions for two evolutionary and functionally related transcription factors, CCCTC-binding factor (zinc finger protein) (CTCF) and its paralogue CTCF-like factor, also denoted Brother of the Regulator of Imprinted Sites (CTCFL/BORIS).
34	24658009	CTCF, a chromatin modeling- and transcription factor, is normally expressed in a ubiquitous fashion, while CTCFL/BORIS is restricted to the testis.
35	24658009	In cancer, CTCF is thought to be a tumor suppressor, while CTCFL/BORIS has been suggested as an oncogene.
36	24658009	Thus, CTCF and CTCFL/BORIS are found to diverge in the different subtypes of endometrial cancer, with CTCFL/BORIS activation through demethylation from precursors to metastatic lesions.
37	24658009	We thus propose, CTCFL/BORIS as an Epi-driver gene in endometrial cancer, suggesting a potential for future vaccine development.