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Akciğer kanserlerinde survivin geninin metilasyon değişimleri ve gen ifadesine etkisinin araştırılması
(2015) Budak, Metin; Sipahi, Tammam; Yalçın, Ömer; Ünlü, Ayhan
[Abstract Nıt Available]
Association of clinicopathological features with E-cadherin (CDH1) gene-160 C>A promoter polymorphism in Turkish colorectal cancer patients
(Wolters Kluwer Medknow Publications, 2019) Bahadir, Anzel; Eral, Gokalp; Budak, Metin; Shimamoto, Fumio; Korpinar, Mehmet Ali; Erdamar, Sibel; Tuncel, Handan
Background and Aim of Study: The role of E-cadherin (CDH1) gene-160 C>A (rsl 6260) promoter polymorphism in colorectal cancer (CRC) still remains inconclusive. The aim of this study is to investigate the associations between the CDH1 -160 C>A polymorphism with the susceptibility and clinicopathological development of CRC in the Turkish patients. To our knowledge, this is the first report examining the role of CDH1 polymorphism in Turkish CRC patients. Materials and Methods: A total of 92 colorectal carcinoma cases (including 62 colon and 30 rectal cancer patients) and the corresponding adjacent normal tissues as controls were studied. The polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism analysis. Clinicopathological features including patient's age, gender, tumor stage, and tumor location (colon/ rectum) were compared statistically with the polymorphism status. Results: There was no significant difference in both genotype and allele frequencies of the CDH1 polymorphism between colorectal tumor cases and normal samples (P = 0.472 and 0.508, respectively). Furthermore, no significant associations were observed between the CDH1 polymorphism status and age, gender, tumor stage, and tumor location of the colorectal tumor cases (all P>0.05). Conclusions: These results indicate that CDH1 -160 C>A polymorphism does not contribute to the genetic susceptibility of CRC and the polymorphism may not be a direct effect on the progression of the disease in Turkish CRC patients.
The association of gene polymorphisms of the angiotensin- converting enzyme and angiotensin II receptor type 1 with ischemic stroke in Turkish subjects of Trakya region
(2009) Sipahi, Tammam; Güldiken, Babürhan Feyzullah; Güldiken, Sibel; Üstündağ, Sedat; Turgut, Nilda; Budak, Metin; Şener, Seralp
Amaç: Bu çalışmanın amacı, Trakya bölgesinde yaşayan iskemik inme geçirmiş hastalarda ACE insersiyon/delesyon (I/D) ve AT1R (A1166C) gen polimorfizmlerinin sıklığını, vasküler risk faktörleri ve inme alt-grupları ile ilişkisini araştırmaktır. Hastalar ve Yöntemler: Çalışmaya 162 iskemik inme geçirmiş hasta ile 146 sağlıklı olgu alındı. İskemik inme hastaları, ORG 10172 Akut İnme Tedavisi (TOAST) kriterlerine göre büyük ve küçük damar hastalığı olarak inme alt gruplarına ayrıldı. ACE I/D polimorfizmi polimeraz zincir reaksiyonu (PZR), AT1R (A1166C) gen polimorfizmi ise PZR ve restriksiyon fragment uzunluk polimorfizmi (RFLP) yöntemleri kullanılarak yapıldı. Bulgular: Hasta grubundaki ACE I/D genotip dağılımı (DD=34.0%, ID=50.0%, II=16.0%), kontrol grubu ile karşılaştırıldığında (DD=34.3%, ID=49.7%, II=16.1%) fark bulunmadı. Ayrıca hasta grubundaki AT1R (A1166C) genotip dağılımları ile (AA=58.0%, CA=34.6% ve CC=7.4%) kontrol grubu ile karşılaştırıldığında (AA=60.1%, CA=35.7% ve CC=4.2%) anlamlı fark saptanmadı. Her iki inme alt grubu arasında ACE I/D ve AT1R (A1166C) polimorfizmlerinin dağılımı açısından farklılık bulunmadı. Sonuç: Çalışmamızda Trakya bölgesinde yaşayan insanlarda ACE I/D ve AT1R (A1166C) gen polimorfizmlerinin iskemik inme gelişmesinde genetik risk faktörleri olmadıkları belirlendi.
The Association of Gene Polymorphisms of the Angiotensin-Converting Enzyme and Angiotensin II Receptor Type 1 with Ischemic Stroke in Turkish Subjects of Trakya Region
(Aves Yayincilik, Ibrahim Kara, 2009) Sipahi, Tammam; Guldiken, Baburhan; Guldiken, Sibel; Ustundag, Sedat; Turgut, Nilda; Budak, Metin; Cakina, Suat
Objectives: The aim of this study was to investigate the frequency of ACE insertion/deletion (I/D) and AT1R (A1166C) gene polymorphisms in ischemic stroke patients in Trakya region and the relation between these gene polymorphisms and stroke subtypes and vascular risk factors. Patients and Methods: The study involved 162 patients with ischemic stroke and 146 control subjects. Ischemic stroke patients were divided into large and small vessel disease subgroups according to ORG 10172 in Acute Stroke Treatment TOAST criteria. The ACE I/D polymorphism was investigated using polymerase chain reaction (PCR), and the AT1R (A1166C) polymorphism was identified using PCR and restriction fragment length polymorphism (RFLP) assay. Results: The ACE I/D genotype distribution in patients (DD=34.0%, ID=50.0%, II=16.0%) did not differ from those in controls (DD=34.3%, ID=49.7%, II=16.1%). The AT1R A1166C genotype distribution in patients (AA=58.0%, CA=34.6%, CC=7.4%) did not significantly differ from those in controls (AA=60.1%, CA=35.7%, CC=4.2%). There was also no difference among the stroke subgroups regarding the distribution of ACE I/D and AT1R (A1166C) polymorphisms. Conclusion: Our results show that ACE I/D and AT1R (A1166C) gene polymorphisms were not genetic risk factors for ischemic stroke in subjects in Trakya region.
A comparative histopathological and immunohistochemical study of Survivin and Ki-67 proteins in glial tumours
(Taylor & Francis Ltd, 2019) Topyalin, Nur; Budak, Metin; Ozbay, Nurver; Yildiz, Mustafa; Kaner, Tuncay; Aydin, Abdullah; Gezen, Ahmet Ferruh
Survivin is a bifunctional protein which regulates cell division and inhibits apoptosis. Survivin is a member of the inhibitor of apoptosis protein (IAP) family. Expression of survivin has been shown to be responsible for apoptosis and resistance to ionizing radiation. The aim of the present study was to investigate the association between -31 G/C promoter polymorphism, survivin protein and glial tumour grading, and to compare survivin versus Ki-67 as a marker. In this study, DNA was isolated from paraffin-embedded sections of 29 patients diagnosed with glial tumours. Survivin gene promoter -31 G/C polymorphism was investigated using PCR-RFLP. For the analysis, 10 mu m sections were stained with survivin protein and Ki-67 antibody. Immunohistochemical staining was performed. Survivin showed a positive correlation with Ki-67 (r = 0.604; p = 0.001). The tumour grades correlated with survivin; however, the relationship was not statistically significant (r = 0.345; p > 0.05). We found a significant correlation between tumour grades and Ki-67 (r = 0.663; p < 0.01), suggesting that Ki-67 is a more sensitive marker compared to survivin.
DNA methylation of the prestin gene and outer hair cell electromotile response of the cochlea in salicylate administration
(Tubitak Scientific & Technological Research Council Turkey, 2017) Bulut, Erdogan; Budak, Metin; Ozturk, Levent; Turkmen, Mehmet T.; Uzun, Cem; Sipahi, Tammam
Background/aim: Activity of the prestin gene may have a role in the pathogenesis of salicylate-induced ototoxicity. We investigated DNA methylation for prestin gene exon 1 in salicylate-injected guinea pigs. Materials and methods: Fifteen guinea pigs (30 ears) underwent audiological evaluation including 1000 Hz probe-tone tympanometry and a distortion product otoacoustic emission (DPOAE) test. The animals were randomly divided into three groups. Groups 2 (8 ears) and 3 (14 ears) were injected with intramuscular saline and sodium salicylate (200 mg/kg), respectively twice daily for 2 weeks. Group 1 (8 ears) received no injection. DPOAE measurements were performed at baseline; after 1, 2, 4, and 8 h (acute effect); and after 1 and 2 weeks (chronic effect). After audiological measurements, the animals were sacrificed for DNA isolation. Results: While a significant decrease (P < 0.01) was found for the acute effect in all frequencies in Group 3 according to baseline measurements, there was no difference in terms of chronic effect. DNA methylation increased during the acute phase of salicylate administration, whereas it returned to initial levels during the chronic phase. Conclusion: Salicylate-induced changes in DPOAE responses may be related to prestin-gene methylation. These results may have important implications for salicylate ototoxicity.
DNA methylation of the prestin gene and outer hair cell electromotileresponse of the cochlea in salicylate administration
(2017) Bulut, Erdoğan; Budak, Metin; Öztürk, Levent; Türkmen, Mehmet T.; Uzun, Cem; Sipahi, Tammam
Background/aim: Activity of the prestin gene may have a role in the pathogenesis of salicylate-induced ototoxicity. We investigated DNA methylation for prestin gene exon 1 in salicylate-injected guinea pigs. Materials and methods: Fifteen guinea pigs (30 ears) underwent audiological evaluation including 1000 Hz probe-tone tympanometry and a distortion product otoacoustic emission (DPOAE) test. The animals were randomly divided into three groups. Groups 2 (8 ears) and 3 (14 ears) were injected with intramuscular saline and sodium salicylate (200 mg/kg), respectively twice daily for 2 weeks. Group 1 (8 ears) received no injection. DPOAE measurements were performed at baseline; after 1, 2, 4, and 8 h (acute effect); and after 1 and 2 weeks (chronic effect). After audiological measurements, the animals were sacrificed for DNA isolation. Results: While a significant decrease (P < 0.01) was found for the acute effect in all frequencies in Group 3 according to baseline measurements, there was no difference in terms of chronic effect. DNA methylation increased during the acute phase of salicylate administration, whereas it returned to initial levels during the chronic phase. Conclusion: Salicylate-induced changes in DPOAE responses may be related to prestin-gene methylation. These results may have important implications for salicylate ototoxicity.
Evaluation of Relationship Between SOD1 50-bp Deletion Gene Polymorphism, Cu, Zn Level, and Viscosity in Postmenopausal Osteoporosis Patients with Vertebral Fractures
(Springernature, 2023) Soyocak, Ahu; Doganer, Fulya; Ergun, Dilek Duzgun; Budak, Metin; Cosan, Didem Turgut; Ozgen, Merih
Oxidative stress plays a role in the pathogenesis of bone loss, causing low bone mineral density (BMD) and associated osteoporotic fractures. In our study, we aimed to investigate the relationship of SOD1 50-bp insertion( Ins)/deletion( Del) polymorphism that is involved in oxidative stress metabolism, Cu and Zn element concentrations, and plasma viscosity level, with postmenopausal osteoporosis and related vertebral fractures. The study included 167 voluntary individuals. The 50- bp Ins/Del polymorphism of SOD1 was determined by allele-specific PCR. Plasma Cu and Zn levels were measured by atomic absorption spectrophotometry (AAS). The plasma viscosity was determined using the Harkness Capillary Viscometer device. In our study, the distribution of SOD1 promoter 50-bp Ins/Del polymorphism did not indicate a significant difference between the groups and in postmenopausal osteoporosis patients with and without fractures (p > 0.05). The Ins/Ins genotype was found to be common in individuals in both groups. The Cu and Zn levels of the study group were found to be between the normal reference values (p > 0.05). It was determined that plasma viscosity increased significantly in the group of osteoporotic patients and in patients with postmenopausal osteoporosis with fractures (p < 0.01). In addition, plasma viscosity was found to significantly increase in patients with Ins/Ins genotype and fractures (p < 0.01). Postmenopausal osteoporosis and associated vertebral fracture were found not to be directly related to SOD1 50-bp polymorphism and Cu and Zn element levels. Plasma viscosity levels were found to increase due to the increase in oxidative stress products. Further studies are needed to clarify the roles and relationships of SOD genes and trace elements in the development of postmenopausal osteoporosis and vertebral fracture.
Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in Turkish patients with ischemic stroke
(Springer, 2009) Guldiken, Baburhan; Sipahi, Tammam; Guldiken, Sibel; Ustundag, Sedat; Budak, Metin; Turgut, Nilda; Ozkan, Hulya
The low plasma nitric oxide concentrations and reduced vascular reactivity are considered major proatherogenic mechanisms in cardiovascular diseases. The present study aimed to assess the allelic frequency and the genotypic distribution of the Glu298Asp gene polymorphism at exon 7 of endothelial nitric oxide synthase (eNOS) gene in Turkish ischemic stroke patients compared to appropriate healthy controls, and to correlate the genetic findings with stroke subtypes. The study population included 146 (75 males, 71 females) patients with ischemic stroke which were categorized according to the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) and 133 (34 males, 99 females) healthy subjects. The eNOS polymorphism was identified with a PCR followed by RFLP with the restriction enzyme BanII. Genotypes were defined as GG, GT, and TT according to the presence of the G and T alleles. In this case-control study, we did not find any significant difference in either the genotypic distribution or allelic frequency of Glu298Asp gene polymorphism between the patients and the controls. In addition, there was also no significant difference for the genotype distribution and the allelic frequency among the stroke subtypes. The results suggested the lack of the association between the Glu298Asp gene polymorphism and ischemic stroke or subtypes of ischemic stroke in the Turkish population.
Hipertansiyonlu hastalarda ACE gen polimorfizminin araştırılması
(Trakya Üniversitesi Sağlık Bilimleri Enstitüsü, 2006) Budak, Metin; Sipahi, Tammam
Hipertansiyon, önemli bir sağlık problemidir. Kan basıncı ve tuz dengesi üstündeki renin-angiotensin sistemi sayesinde düzenlenir. Angiotensin Converting Enzim (ACE)'de bu sisteme ait bir enzimdir. ACE İnsertion / Deletion (I/D) polimorfizmi çeşitli kardiovasküler hastalıklarda önemli olduğu gösterilmiştir. Fakat ACE I/D polimorfizminin hipertansiyonda rolü olduğunu gösteren çalışmalar olmakla birlikte hipertansiyona etkisi olmadığını gösteren çalışmalarda mevcuttur. Çalışmamızda 79 hipertansiyonlu hasta ve 38 kontrol gurubunda Polimeraz Zincir Reaksiyonu (PCR) ve agaroz jel sistemi ile ACE I/D polimorfizmi çalışıldı. Erkek hasta ve kontrol guruplarında genotip dağılımları normal bulundu. ACE Deletion / Deletion (DD) genotipi kadın hasta gurubunda (%35.5) anlamlı şekilde kontrol gurubuna göre yüksek bulundu (%21.4). Bu sonuçlara göre ACE DD genotipi kadınlarda hipertansiyon ile ilişkili olduğu gösterildi ancak bu fark erkeklerde gösterilemedi.
Importance of p53, bcl-2, p21WAF1 and PCNA positivities in renal angiomyolipomas
(Allied Acad, 2017) Budak, Metin; Yalcin, Omer; Usta, Ufuk; Tokuc, Burcu
Angiomyolipomas are tumors of the kidneys which are often benign in character with a potential for malignant transformation. The benign-malign distinction in these tumors can be made only with clinical follow-up as they exhibit the same microscopic appearance. In the present study, immunohistochemical investigation has been performed for p53, p21(WAF1), PCNA and bcl-2, which may be markers for the histological distinction of benign and malignant cases. The p53, p21WAF1, PCNA and bcl-2 investigations in 10 tumor tissues with AML revealed significantly higher p53 positivity in 3 patients. The clinical follow-up of these three patients showed malignant progression. In conclusion, we believe that p53 positivity may be an appropriate marker for the benign-malign distinction in AML tumors.
Larink kanserlerinde smad4 metilasyonu yönünden epigenetik bir yaklaşım
(Sağlık Bilimleri, 2020) Temiz, Alp Selahattin; Budak, Metin
Mothers Against Decapentaplegic Homolog 4 -MADH4 ya da SMAD4 olarak da bilinir- bir tümör baskılayıcı gen bölgesidir. Bu türden tümör baskılayıcı gen bölgelerinin hipermetilasyonu, organizmanın kendisinin kansere karşı ortaya koyduğu mücadelede zayıflığa yol açabilir. Pek çok bölgede gelişen kanser türünde SMAD4 metilasyonu incelenegelmektedir. Bilhassa gastrointestinal kanal ve pankreas ile ilişkili kanserlerin SMAD4 hipermetilasyonu ile ile ilişkili olduğu bulunmuştur. Çok sayıda araştırmacının SMAD4 ifadesi üzerine odaklanmasına karşın, larinks kanserlerinde metilasyon spesifik polimeraz zincir reaksiyonuna göre bant yoğunluklarının ölçümü esasına dayanan hiçbir yayın bulunamamıştır. Bu çalışma, larinks kanserlerinde SMAD4 metilasyonunun rolünü aydınlatmayı hedeflemiştir. Bu çalışmaya larinks kanseri tanısı almış otuz dört hasta dahil edilmiştir. Söz konusu araştırmayı gerçekleştirebilmek adına biyopsi materyallerinden elde edilmiş tümör dokularından ve bukkal swablar ile toplanan kontrol dokularından DNA izolasyonu yapıldı. Spektrofotometrik yöntemlerle, izole edilmiş DNA örneklerinin miktarları ve saflıkları ölçüldü. Metilasyon spesifik polimeraz zincir reaksiyonu için bisülfit modifikasyonu gerçekleştirildi. Çoğaltılan tüm DNA numuneleri yatay elektroforez uygulaması için bir agaroz jele yüklendi. Bantlar ultraviyole görüntüleme kamerası altında kayıt altına alındı ve bant yoğunlukları uygun bir bilgisayar yazılımı ile ölçüldü. Elde edilen tüm sonuçlar istatistik analiz yazılımı ile incelendi. Bu araştırma, larinks kanseri tanısı almış hastaların tümör dokularındaki SMAD4 gen bölgesindeki metilasyon düzeyinin kontrol dokularına kıyasla istatistiksel olarak anlamlı düzeyde artış gösterdiğini açıkça ortaya koymaktadır (z=-2,265 ve p=0,023).
Lipoprotein(a) Gene Polymorphism Increases a Risk Factor for Aortic Valve Calcification
(Mdpi, 2019) Ozkan, Ugur; Ozcelik, Fatih; Yildiz, Mustafa; Budak, Metin
Calcific aortic valve disease (CAVD) is a multifactorial condition. Both environmental and genetic factors play an important role in its etiology. CAVD exhibits a broad spectrum, varying from mild valve thickening to severe valve calcification and stenosis. Progression of the disease consists of chronic inflammation, lipoprotein deposition, and active leaflet calcification. It is a process similar to coronary artery disease. In this study, we investigated Lp(a) levels and gene polymorphisms associated with calcific aortic stenosis from blood samples after echocardiography in the evaluation of 75 patients diagnosed with CAVD and 77 controls. Blood tests were run in our laboratory to rule out certain risk factors before echocardiography examination. A significant association among smoking, elevated LDL level and creatinine, low albumin levels, Lp(a) level, rs10455872, and rs3798220 polymorphisms may be considered genetic risk factors for the development of calcific aortic stenosis.
Methylation status, mRNA and protein expression of the SMAD4 gene in patients with non-melanocytic skin cancers
(Springer, 2023) Urun, Yildiz Gursel; Budak, Metin; Keskin, Elif Usturali
Background SMAD4 is a potent tumor suppressor. SMAD4 loss increases genomic instability and plays a critical role in the DNA damage response that leads to skin cancer development. We aimed to investigate SMAD4 methylation effects on mRNA and protein expression of SMAD4 in cancer and healthy tissues from patients with basal cell carcinoma (BCC), cutaneous squamous cell carcinoma (cSCC), and basosquamous skin cancer (BSC). Methods and results The study included 17 BCC, 24 cSCC and nine BSC patients. DNA and RNA were isolated from cancerous and healthy tissues following punch biopsy. Methylation-specific polymerase chain reaction ( PCR) and real-time quantitative PCR methods were used to examine SMAD4 promoter methylation and SMAD4 mRNA levels, respectively. The percentage and intensity of staining of the SMAD4 protein were determined by immunohistochemistry. The percentage of SMAD4 methylation was increased in the patients with BCC (p = 0.007), cSCC (p = 0.004), and BSC (p = 0.018) compared to the healthy tissue. SMAD4 mRNA expression was decreased in the patients with BCC (p.0.001), cSCC (p.0.001), and BSC (p = 0.008). The staining characteristic of SMAD4 protein was negative in the cancer tissues of the patients with cSCC (p = 0.00). Lower SMAD4 mRNA levels were observed in the poorly differentiated cSCC patients ( p = 0.001). The staining characteristics of the SMAD4 protein were related to age and chronic sun exposure. Conclusions Hypermethylation of SMAD4 and reduced SMAD4 mRNA expression were found to play a role in the pathogenesis of BCC, cSCC, and BSC. A decrease in SMAD4 protein expression level was observed only in cSCC patients. This suggests that epigenetic alterations to the SMAD4 gene are associated with cSCC.
No mutation effect of 50 Hz sinusoidal magnetic field on beta catenin gene phosphorylation site in N-methyl-N-nitrosourea (MNU) induced colon tumor model
(Natl Inst Science Communication-Niscair, 2023) Budak, Metin; Kilic, Mahmut Alp; Kalkan, Tunaya; Tuncel, Handan
The dysregulation of beta-catenin, a key regulator of cadherin-mediated cell adhesion and crucial for embryonic development and adult tissue processes, has been implicated in various cancers, including colon cancer. Meanwhile, there have been longstanding concerns about the potential carcinogenic effects of magnetic fields. In this study, we investigated the possible relationship between beta-catenin dysfunction and 50 Hz sinusoidal magnetic fields (SMF) using an animal model of N-methyl-N-nitrosourea (MNU)-induced rat colon tumors. To assess beta-catenin phosphorylation, genomic DNA was extracted from 58 samples using a commercial extraction kit, and the target gene region corresponding to an important phosphorylation site of beta-catenin was amplified via polymerase chain reaction (PCR). The amplified samples were subsequently analyzed using the single-strand conformation polymorphism (SSCP) method to detect any differences between the experimental groups. Surprisingly, our results revealed no significant differences in beta-catenin gene phosphorylation sites among the groups. These findings suggest that 50 Hz SMF exposure may not directly impact beta-catenin dysfunction in the context of MNU-induced rat colon tumors. Implications of these results and avenues for further research are discussed.
Poli ADP-Riboz Polimerazlarda ve ADP-Ribozilleyen Toksinlerde Nikotinamid Adenin Dinu?kelotidi Tanıyan Ortak Motifin Üç Boyutlu Yapısının Belirlenerek Bu Ortak Motifin Etkileşim Arayu?zu?nu?n ve Bağlanma Enerjileri Yu?ksek Sıcak Noktalarının Kuramsal ve Deneysel Yöntemlerle Araştırılması
(2016) Ünlü, Ayhan; Bektaş, Muhammet; Sipahi, Tammam; Budak, Metin
ADP-ribozilleyen toksinleri (ADPRT) ve poli ADP-riboz polimerazları (PARP) nikotinamid adenin dinu?kleotidi (NAD) substrat olarak kullanan iki ana sınıfıdır. Bunlar NAD’nın nikotinamid ve ADP-riboz’a dönu?şu?mu?nu? katalize eden enzimleri metabolize eder ve ADP-ribozun hedef proteine transferini sağlar. PARPlar çoğu ökaryotta her yerde bulunan enzimlerdir ve post-translasyonel protein modifikasyonlarında işlev gördu?kleri bilinmektedir. Burada ADP-riboz parçası NAD’tan belirli substratlara transfer edilir. İnsan genomunda on yedi putatif PARP sekansı belirlenmiştir. Genom korumasında, transkripsyonal du?zenlemede, DNA hasar sensörlerinde ve onarımında, enerji metabolizmasında, hu?cre çoğalmasında ve farklılaşmasında, apoptozda görev alırlar. PARP’ların aşırı aktivasyonu hu?credeki NAD+ ve ATP’nin tu?ketilmesine neden olur ve iltihaplı yaralara, hu?crede fonksiyon bozukluğuna ve sonunda nekrotik hu?cre ölu?mlerine yol açabilir. Kanser tedavilerinde PARP’ların inhibisyonu sonucunda DNA onarımının arttıracağı ve bu durumun antikanser terapilerinin etkilerini arttırabileceği du?şu?nu?lmektedir. PARP’ların yapılarının ve etkinliklerinin anlaşılması inflamasyon, dejeneretif, vasku?lar ve kanser gibi hastalıkların terapisine yönelik ilaç geliştirmelerinde önem arzetmektedir. ADPRT’lar, tehlikeli ve ölu?mcu?l bu?yu?k bir toksin ailesidir. Bunlar patojenik bakteriler tarafından salgılanır ve insanın hedef proteinlerinin fonksiyonlarını engellerler. Yapı temelli çoklu sekans hizalamalarına dayalı olarak ADPRT ailesi iki grupta sınıflandırılırlar. AB grubu toksinleri, ökaryotik elongasyon faktör 2 (eEF2)’yi ADP-ribozilleyerek protein sentezini inhibe eder. Bu grubun u?yeleri arasında DT, ekzotoksin A (ETA) ve cholix toksin vardır. CT grubu toksinleri, konakçı organizmalardaki önemli işlevleri bulunan proteinleri hedef alırlar. Örneğin bitkisel böcek ilacı protein 2 (VIP2), iota ve botilinum C2 toksinleri aktini ADP-ribozilleyerek polimerizasyonunu (F-aktin) oluşumunu engeller. PARP ve ADPRT enzimleri, farklı çeşitlilikte fonksiyonlar ve du?şu?k sekans kimlikleri gösterse de, ortak yapısal ve işlevsel özellikler paylaşırlar. Gılikohidrolaz ve transferaz aktivitelerine sahiptirler. İlk olarak, ortak bir reaksiyon, yani ADP-ribozilasyonu katalize ederler. Böylece nikotinamid ve NAD+’ın N-ribozu arasındaki C-N bağı kopar ve sonra ADP-riboz parçası hedef proteine transfer edilir. İkinci olarak, yapı itibarıyla benzer katalitik bölgelere sahiplerdir. Biz çalışmamızda Bu projede ADPRT’ler ve PARP’ların, NAD’yi tanıyan ortak motiflerin u?ç boyutlu yapılarını, etkileşim arayu?zlerini, motiflerdeki bağlanma enerjilerini, diğer amino asitlere göre daha yu?ksek olan sıcak noktalarını deneysel ve kuramsal çalışmalar yaparak belirledik.
A potential biomarker for individuals of chronic subjective tinnitus with normal hearing: Serum prestin levels
(Wiley, 2023) Bulut, Erdogan; Budak, Metin; Guven, Selis Gulsevin; Atilgan, Emre; Uzun, Cem
[Abstract Not Available]
SMAD4 Gene Methylation May Be Effective in Adenocarcinoma Lung Cancers
(Galenos Yayincilik, 2021) Budak, Metin
Objective: In this study, we aimed to investigate the effect of promoter region methylation of small mothers against decapentaplegic 4 (SMAD4) gene in adenoma type lung cancer cases. Adenocarcinoma and squamous type carcinomas are the most common types of lung cancer. SMAD4 gene is an intracellular signal protein. The protein of this gene, which is one of the transcription factors, functions in tissue homeostasis during embryonic development and has effects in the cancer process. Methods: In this retrospective study, a total of 40 samples including 20 paraffin-embedded tumor tissues of 20 patients with adenocarcinoma lung cancer and normal lung tissue of the same patients were included. After DNA isolation from this paraffin-embedded adenocarcinoma lung tumor tissue and its normal counterparts, methylation specific polymerase chain reaction followed by agarose gel imaging methods were applied to investigate the SMAD4 promoter methylation after bisulfite modification. Results: As a result of our study, an increased presence of methylation in the promoter region of the SMAD4 gene in the tumor tissue of a total of 12 (60%) of 20 adenocarcinoma cases compared to normal tissue was detected. A statistically significant increase in methylation rate of approximately 25-45% was found in tumor tissues of these cases compared to normal tissues (p<0.05). Conclusion: As a result of our study, we suggested that SMAD4 gene methylation may be a tumor marker for lung cancers and may contribute to the development of cancer by inhibiting SMAD4 protein expression by gene methylation and disrupting the intracellular signal pathway.

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