An Overview of Synergistic Data Tools for Biological Scrutiny

Olender, Tsviya; Edgar, Ron; Stelzer, Gil; Nativ, Noam; Rosen, Naomi; Shtrichman, Ronit; Mazor, Yaron; West, Michael; Keydar, Ifat; Rappaport, Noa; Belinky, Frida; Warshawsky, David; Lancet, Doron

doi:10.1002/ijch.201200094

Cited by 5 publications

(5 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sp1 has zinc finger motifs by which it binds directly to DNA at the GC box element by the established consensus sequence 5Ј-GGGGCGGGG or (G/T)-GGGCGG(G/A)(G/A)(C/T)-3Ј (11). Multiple studies have confirmed that mutation of this consensus sequence leads to reduced promoter activation and expression of target genes (12)(13)(14)(15).…”

mentioning

confidence: 99%

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Bhattacharyya

Feferman

Tobacman

2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Mechanism by which Wnt expression was increased by carrageenan exposure was unknown. Results: Sp1 activated Wnt9A transcription through changes in arylsulfatase B, chondroitin 4-sulfation, and galectin-3. Conclusion: Decline in arylsulfatase B leads to transcriptional effects mediated by Sp1 and galectin-3. Significance: Extracellular events can regulate transcription through changes in arylsulfatase B and chondroitin 4-sulfation.

show abstract

mentioning

confidence: 99%

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Bhattacharyya

Feferman

Tobacman

2014

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Molecular structure of doi: 10.7243/2052-434X-4-1 the fusion between in PDGFRα and ETV6 was examined in a few cases of t(4;12). Curtis et al, [22] reported an MPN with eosinophilia and t(4;12) in which ETV6 was translocated to the 5'-of an intact WW domain of PDGFRα; this patient responded to imatinib. Yoshida et al, [40] reported an another case in which ETV6 fused to the C-terminus of PDGFRα and the patient did not respond to imatinib.…”

Section: Discussionmentioning

confidence: 87%

“…Evaluation of gene function for each of these genes was conducted using GeneCards encyclopedia (www.genecards.org), and annotated by the area of interest utilizing UCSC, Ensemble, Uniprot, MGI mutation, GO/KEGG pathway, OMIM diseases, and MalaCards diseases [22]. This evaluation indicated that 6 genes, E2F3, GMNN, CHTF18, TELO2, CCNF and PKMYT1 have a cell cycle function; 7 genes, TXNDC5, SOX4, PRL, AXIN1, ZNF598, NRG3 and DNAJA3 have a function related to apoptosis; 8 genes, DEK, ID4, TRIM38, ZMIZ1, IL32, CREBBP, GLIS2 and PGP have been reported to be related to established leukemic entities; and 8 genes, PKMYT1, IL32, RIPK1, PRPF4B, NRG3, MLST8, PGP and PDPK1 have been linked to tyrosine kinase signaling pathways.…”

Section: Cytogenetics and Fishmentioning

confidence: 99%

A unique rearrangement of PDGFRα and ETV6 in a patient with acute myeloid leukemia with myelodysplasia-related changes progressed from chronic myelomonocytic leukemia

Koduru¹,

Guruju²,

Patel³

et al. 2016

Hematol Leuk

View full text Add to dashboard Cite

Platelet derived growth factor receptor alpha (PDGFRα) undergoes different types of rearrangements creating fusion genes in myeloid neoplasms. Cryptic deletion at 4q12 creating FIP1L1/PDGFRα fusion is the most frequent and is associated with hypereosinophilia. The other infrequent but recurrent abnormality involving PDGFRα seen in myeloid neoplasms is a t(4;12)(q12;p13), which creates a fusion gene with ETV6 and activates ETV6 via the tyrosine kinase domain of the PDGFRα. We characterized a new t(4;12;6) translocation which developed during transformation to acute myeloid leukemia (AML) in a patient with chronic myelomonocytic leukemia (CMML). Standard G-band karyotype analysis and fluorescence in-situ hybridization study (FISH) analysis with a tricolor 4q12 probe and ETV6 was performed on the bone marrow (BM) involved by AML. The karyotype showed a t(4;12;6)( q12;p13;p21.3). FISH showed fusion between PDGFRα and ETV6. Patient did not respond to treatment with imatinib or to standard induction chemotherapy for AML, and expired 11 months from diagnosis. This is the first report of a variant t(4;12;6) and ETV6/PDGFRα fusion that developed during transition from CMML to AML and did not respond to imatinib.

show abstract

“…For the above members of the UPR, a summary of the gene/protein names and their synonyms as well as their primary subcellular localization was compiled from www.genecards.org (Olender et al 2013) and is presented in Table 2.…”

Section: Discussionmentioning

confidence: 99%

Oxygen–Glucose Deprivation (OGD) Modulates the Unfolded Protein Response (UPR) and Inflicts Autophagy in a PC12 Hypoxia Cell Line Model

et al. 2015

View full text Add to dashboard Cite

Hypoxia is the lack of sufficient oxygenation of tissue, imposing severe stress upon cells. It is a major feature of many pathological conditions such as stroke, traumatic brain injury, cerebral hemorrhage, perinatal asphyxia and can lead to cell death due to energy depletion and increased free radical generation. The present study investigates the effect of hypoxia on the unfolded protein response of the cell (UPR), utilizing a 16-h oxygen-glucose deprivation protocol (OGD) in a PC12 cell line model. Expression of glucose-regulated protein 78 (GRP78) and glucose-regulated protein 94 (GRP94), key players of the UPR, was studied along with the expression of glucose-regulated protein 75 (GRP75), heat shock cognate 70 (HSC70), and glyceraldehyde 3-phosphate dehydrogenase, all with respect to the cell death mechanism(s). Cells subjected to OGD displayed upregulation of GRP78 and GRP94 and concurrent downregulation of GRP75. These findings were accompanied with minimal apoptotic cell death and induction of autophagy. The above observation warrants further investigation to elucidate whether autophagy acts as a pro-survival mechanism that upon severe and prolonged hypoxia acts as a concerted cell response leading to cell death. In our OGD model, hypoxia modulates UPR and induces autophagy.

show abstract

An Overview of Synergistic Data Tools for Biological Scrutiny

Cited by 5 publications

References 52 publications

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

A unique rearrangement of PDGFRα and ETV6 in a patient with acute myeloid leukemia with myelodysplasia-related changes progressed from chronic myelomonocytic leukemia

Oxygen–Glucose Deprivation (OGD) Modulates the Unfolded Protein Response (UPR) and Inflicts Autophagy in a PC12 Hypoxia Cell Line Model

Contact Info

Product

Resources

About