TOP TEN perturbations for 1552499_a_at (Homo sapiens)

Organism: Homo sapiens
Gene: 1552499_a_at
Selected probe(set): 1552498_at
Platform: Affymetrix Human Genome U133 Plus 2.0 Array

Expression of 1552499_a_at (1552498_at) across 6540 perturbations tested by GENEVESTIGATOR:

HIF-2a depletion study 1 (hypoxia; HK2) / HIF-1a depletion study 2 (hypoxia; HK2)

Relative Expression (log2-ratio):1.264298
Number of Samples:3 / 3
Experimental HIF-2a depletion study 1 (hypoxia; HK2)
Proximal tubule epithelial cell line HK-2 with shRNA-mediated stable knock-down of HIF-2a (Hypoxia-inducible factor 2-alpha) 24 hours after treatment with hypoxia (1% O2). HK-2 cells were cultured in DMEM/F-12 supplemented with 10% fetal calf serum (FCS), 1% ITS, hydrocortisone, and antibiotics. The cells were incubated at 37 °C.
Control HIF-1a depletion study 2 (hypoxia; HK2)
Proximal tubule epithelial cell line HK-2 with shRNA-mediated stable knock-down of HIF-1a (Hypoxia-inducible factor 1-alpha) 24 hours after treatment with hypoxia (1% O2). HK-2 cells were cultured in DMEM/F-12 supplemented with 10% fetal calf serum (FCS), 1% ITS, hydrocortisone, and antibiotics. The cells were incubated at 37 °C.

atopic dermatitis study 21 (non-lesional; whole skin) / normal skin tissue

Relative Expression (log2-ratio):-0.99313164
Number of Samples:5 / 6
Experimental atopic dermatitis study 21 (non-lesional; whole skin)
Non-lesional full thickness skin samples isolated from patient with moderate-to-severe atopic dermatitis by laser capture microdissection. Patients' cohort characteristics: 3 males and 2 females; age 27-59 years (mean age: 39.4 years); SCORing of Atopic Dermatitis index (SCORAD) ranging from 45-65; total IgE: 14-1821 kU/l; eosinophilic count: 1.4-11.8 %.
Control normal skin tissue
Full thickness skin samples isolated from healthy subjects by laser capture microdissection.

HIF-1a/HIF-2a depletion study 1 (normoxia; AB81) / control AB81 cell sample (normoxia)

Relative Expression (log2-ratio):-0.85547495
Number of Samples:3 / 3
Experimental HIF-1a/HIF-2a depletion study 1 (normoxia; AB81)
Human podocyte cells AB81 with shRNA-mediated stable knock-down of HIF-1a and HIF-2a (Hypoxia-inducible factor 1-alpha and Hypoxia-inducible factor 2-alpha) 24 hours after treatment with normoxia (20% O2). Conditionally immortalized human podocytes AB81 were cultured under permissive conditions (33 °C) in RPMI-1640 supplemented with 10% FBS, antibiotics, and 1% ITS. Differentiation was induced by thermoshift to 37 °C in 6-well plates.
Control control AB81 cell sample (normoxia)
Human podocyte cell line AB81 treated with normoxia (20% O2) for 24 hours. Conditionally immortalized human podocytes AB81 were cultured under permissive conditions (33 °C) in RPMI-1640 supplemented with 10% FBS, antibiotics, and 1% ITS. Differentiation was induced by thermoshift to 37 °C in 6-well plates.

HIF-1a/HIF-2a depletion study 1 (normoxia; AB81) / HIF-2a depletion study 1 (normoxia; AB81)

Relative Expression (log2-ratio):-0.82880926
Number of Samples:3 / 3
Experimental HIF-1a/HIF-2a depletion study 1 (normoxia; AB81)
Human podocyte cells AB81 with shRNA-mediated stable knock-down of HIF-1a and HIF-2a (Hypoxia-inducible factor 1-alpha and Hypoxia-inducible factor 2-alpha) 24 hours after treatment with normoxia (20% O2). Conditionally immortalized human podocytes AB81 were cultured under permissive conditions (33 °C) in RPMI-1640 supplemented with 10% FBS, antibiotics, and 1% ITS. Differentiation was induced by thermoshift to 37 °C in 6-well plates.
Control HIF-2a depletion study 1 (normoxia; AB81)
Human podocyte cells AB81 with shRNA-mediated stable knock-down of HIF-2a (Hypoxia-inducible factor 2-alpha) 24 hours after treatment with normoxia (20% O2). Conditionally immortalized human podocytes AB81 were cultured under permissive conditions (33 °C) in RPMI-1640 supplemented with 10% FBS, antibiotics, and 1% ITS. Differentiation was induced by thermoshift to 37 °C in 6-well plates.

diclofenac study 7 (24h) / vehicle (PBS) treated HepG2 cell sample

Relative Expression (log2-ratio):0.78711987
Number of Samples:3 / 3
Experimental diclofenac study 7 (24h)
HepG2 cells exposed to 100μM diclofenac in PBS solvent for 24 hours. ATC code:, ,
Control vehicle (PBS) treated HepG2 cell sample
HepG2 cells exposed to 0.5% PBS solvent for 24 hours.

tunicamycin study 2 (2ug/ml; HCT 116) / untreated HCT 116 cell sample

Relative Expression (log2-ratio):-0.7332001
Number of Samples:3 / 3
Experimental tunicamycin study 2 (2ug/ml; HCT 116)
Human colon carcinoma cell line HCT116 was treated with 2 ug/ml tunicamycin for 24 hours in McCOYs 5A medium supplemented with 10% heat inactivated FBS. ATC code:---
Control untreated HCT 116 cell sample
Human colon carcinoma cell line HCT116 was grown in McCOYs 5A medium supplemented with 10% heat inactivated FBS.

HIF-1a depletion study 2 (hypoxia; HK2) / HIF-1a depletion study 2 (normoxia; HK2)

Relative Expression (log2-ratio):-0.6668992
Number of Samples:3 / 3
Experimental HIF-1a depletion study 2 (hypoxia; HK2)
Proximal tubule epithelial cell line HK-2 with shRNA-mediated stable knock-down of HIF-1a (Hypoxia-inducible factor 1-alpha) 24 hours after treatment with hypoxia (1% O2). HK-2 cells were cultured in DMEM/F-12 supplemented with 10% fetal calf serum (FCS), 1% ITS, hydrocortisone, and antibiotics. The cells were incubated at 37 °C.
Control HIF-1a depletion study 2 (normoxia; HK2)
Proximal tubule epithelial cell line HK-2 with shRNA-mediated stable knock-down of HIF-1a (Hypoxia-inducible factor 1-alpha) 24 hours after treatment with normoxia (20% O2). HK-2 cells were cultured in DMEM/F-12 supplemented with 10% fetal calf serum (FCS), 1% ITS, hydrocortisone, and antibiotics. The cells were incubated at 37 °C.

brefeldin A study 1 (0.5ug/ml; HCT 116) / untreated HCT 116 cell sample

Relative Expression (log2-ratio):-0.6477871
Number of Samples:3 / 3
Experimental brefeldin A study 1 (0.5ug/ml; HCT 116)
Human colon carcinoma cell line HCT116 was treated with 0.5 ug/ml brefeldin-A for 24 hours in McCOYs 5A medium supplemented with 10% heat inactivated FBS. ATC code:---
Control untreated HCT 116 cell sample
Human colon carcinoma cell line HCT116 was grown in McCOYs 5A medium supplemented with 10% heat inactivated FBS.

BEZ235 study 1 (3.606 uM) / BKM120 study 1 (IC90; 3.606 uM)

Relative Expression (log2-ratio):0.6259804
Number of Samples:4 / 4
Experimental BEZ235 study 1 (3.606 uM)
A2058 cells treated with 3.606 uM NVP-BEZ235 for 24hours. The concentration corresponding to the IC90 of BKM120. Cells were maintained in DMEM, high glucose, 10% FCS, 1% pyruvate, 2% glutamine. BEZ235 is a mTOR/PI3K inhibitor; alternative names: [NVP-BEZ235] ATC code:---
Control BKM120 study 1 (IC90; 3.606 uM)
A2058 cells treated with BKM120 for 24hours at an IC90 concentration of 3.606 uM. Concentration of IC90 was judged by reduction of pAkt levels (S473P-Akt inhibition). Cells were maintained in DMEM, high glucose, 10% FCS, 1% pyruvate, 2% glutamine. BKM120 is a pan-PI3K inhibitor; alternative names: [buparlisib, NVP-BKM120] ATC code:---

endometriosis study 6 (minimal/mild endo.; pro. MCP) / normal endometrium tissue (pro. MCP)

Relative Expression (log2-ratio):0.6145716
Number of Samples:12 / 20
Experimental endometriosis study 6 (minimal/mild endo.; pro. MCP)
Endometrial tissue samples from women with minimal or mild endometriosis and pelvic pain and/or infertility collected in the proliferative menstrual cycle phase (MCP). Endometriosis was diagnosed based on the revised American Fertility Society classification system. The MCP was determined by endometrial histology, confirmed by estradiol and progesterone serum levels and corroborated by 2 independent bioinformatics methods: clustering in unsupervised whole-transcriptome principal component analysis and cycle phase assignment classifier analysis. Patients with hormonal treatment within previous 3 months and presence of malignancy or major systemic disease were excluded.
Control normal endometrium tissue (pro. MCP)
Normal endometrial tissue samples from women collected in the proliferative menstrual cycle phase (MCP). The MCP was determined by endometrial histology, confirmed by estradiol and progesterone serum levels and corroborated by 2 independent bioinformatics methods: clustering in unsupervised whole-transcriptome principal component analysis and cycle phase assignment classifier analysis.