Yalcin Erzurumlu
Ege University
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Publication
Featured researches published by Yalcin Erzurumlu.
The International Journal of Biochemistry & Cell Biology | 2013
Yalcin Erzurumlu; Fadime Aydin Kose; Oguz Gozen; Devrim Gozuacik; Eric A. Toth; Petek Ballar
p97/VCP is a hexameric AAA type ATPase that functions in a variety of cellular processes such as endoplasmic reticulum associated degradation (ERAD), organelle biogenesis, autophagy and cell-cycle regulation. Inclusion body myopathy associated with Paget disease of the bone and frontotemporal dementia (IBMPFD) is an autosomal dominant disorder which has been attributed to mutations in p97/VCP. Several missense mutations affecting twelve different amino acids have been identified in IBMPFD patients and some of them were suggested to be involved in the observed pathology. Here, we analyzed the effect of all twelve p97/VCP variants on ERAD substrates and their cofactor binding abilities. While all mutants cause ERAD substrate accumulation, P137L mutant p97/VCP differs from other IBMPFD mutants by having a unique solubility profile and subcellular localization. Intriguingly, although almost all mutants exhibit enhanced p47 and Ufd1-Npl4 binding, the P137L mutation completely abolishes p97/VCP interactions with Ufd1, Npl4 and p47, while retaining its gp78 binding. While recombinant R155C mutant protein consistently interacts with both Ufd1 and VIM of gp78, P137L mutant protein lost binding ability to Ufd1 but not to VIM in vitro. The differential impairments in p97/VCP interactions with its functional partners and function should help our understanding of the molecular pathogenesis of IBMPFD.
Scientific Reports | 2017
Yalcin Erzurumlu; Petek Ballar
The endoplasmic reticulum (ER) comprises thirty percent of the newly translated proteins in eukaryotic cells. The quality control mechanism within the ER distinguishes between properly and improperly folded proteins and ensures that unwanted proteins are retained in the ER and subsequently degraded through ER-associated degradation (ERAD). Besides cleaning of misfolded proteins ERAD is also important for physiological processes by regulating the abundance of normal proteins of the ER. Thus it is important to unreveal the regulation patterns of ERAD. Here, we describe that ERAD pathway is regulated by androgen, where its inhibitor SVIP was downregulated, all other ERAD genes were upregulated. Consistently, androgen treatment increased the degradation rate of ERAD substrates. Using several independent techniques, we showed that this regulation is through androgen receptor transactivation. ERAD genes found to be upregulated in prostate cancer tissues and silencing expression of Hrd1, SVIP, and gp78 reduced the in vitro migration and malignant transformation of LNCaP cells. Our data suggests that expression levels of ERAD components are regulated by androgens, that promotes ERAD proteolytic activity, which is positively related with prostate tumorigenesis.
Atlas of genetics and cytogenetics in oncology and haematology | 2012
Yalcin Erzurumlu; Petek Ballar
Review on AMFR (autocrine motility factor receptor), with data on DNA, on the protein encoded, and where the gene is implicated.
Chemical Biology & Drug Design | 2018
Sülünay Parlar; Yalcin Erzurumlu; Recep Ilhan; Petek Ballar Kirmizibayrak; Vildan Alptüzün; Ercin Erciyas
The hydrazones of 4‐hydrazinylpyridinium bearing alkylphenyl groups on pyridinium nitrogen were synthesized and evaluated for their cytotoxic activity against MCF‐7, PC3, U2OS, and HEK293 cell lines by Wst1 cell proliferation assay. Cytotoxic activity results indicated that d derivatives having butylene chain; 4 and 5 series having naphthalene and anthracene ring systems showed high cytotoxic activity (IC50 = 3.27–8.54 μm) on cancer cells. 3d (4‐(2‐(4‐hydroxybenzylidene)hydrazinyl)‐1‐(4‐phenylbutyl)pyridinium bromide) was the most cytotoxic compound with IC50 value of 3.27 μm against MCF‐7. The most active derivatives (1d, 2d, 3d, 4, and 5 series) were selected to investigate for the effects on autophagy by analyzing the expression of autophagy marker proteins. The conversion of LC3‐I to its lipidated form LC3‐II is essential for autophagy and related to autophagosomes. According to our results, all tested compounds except for 3d induced lipidated form LC3‐II accumulation. Then, the effects of the compounds on p62 protein level were also analyzed by the immunoblotting as the autophagy inhibition results in accumulation of p62. Further molecular mechanistic studies including morphological analysis and live–death assays indicated that all tested compounds (1d, 2d, 3d, 4, and 5 series) are potent antitumoral molecules and all except for 3d have potential to inhibit autophagic flux.
Atlas of genetics and cytogenetics in oncology and haematology | 2013
Yalcin Erzurumlu; Recep Ilhan; Oguz Gozen; Petek Ballar
Review on VCP (valosin containing protein), with data on DNA, on the protein encoded, and where the gene is implicated.
Letters in Drug Design & Discovery | 2014
Huseyin Istanbullu; Yalcin Erzurumlu; Petek Ballar Kirmizibayrak; Ercin Erciyas
Journal of Electroanalytical Chemistry | 2016
P. Kara; Yalcin Erzurumlu; P. Ballar Kirmizibayrak; Mehmet Ozsoz
Archive | 2012
Yalcin Erzurumlu; Petek Ballar
Archive | 2017
Yalcin Erzurumlu; Özgür Tağ; Sinem Yılmaz; Petek Ballar; Erdal Bedir
Free Radical Biology and Medicine | 2018
Ayfer Yalcin; Ezgi Turunc; Yiğit Uyanıkgil; Lutfiye Kanit; Mehmet M. Kaplan; Yalcin Erzurumlu; Ege Sevinc