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<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Artificial intelligence and genomic data privacy: Balancing innovation with security</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>1</FirstPage>
			<LastPage>2</LastPage>
			<ELocationID EIdType="pii">8294</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.54335.2217</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Leila</FirstName>
					<LastName>Kohan</LastName>
<Affiliation>Department of Biology, Ars.C., Islamic Azad University, Arsanjan, Iran</Affiliation>
<Identifier Source="ORCID">0000-0001-7124-2849</Identifier>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>09</Month>
					<Day>20</Day>
				</PubDate>
			</History>
		<Abstract>No abstract</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">artificial intelligence</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Privacy</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Genomic Data</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">personalized medicine</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8294_5e10d544ba10cd65e68aa85377c19655.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>The possibility of prognostic and functional values of the 8q24 and 20q13 chromosomal bands in colorectal cancer</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>3</FirstPage>
			<LastPage>10</LastPage>
			<ELocationID EIdType="pii">8296</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.54114.2202</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Seyed Ahmadreza</FirstName>
					<LastName>Siadat</LastName>
<Affiliation>Department of Biology, School of Science, Shiraz University, Shiraz, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>08</Month>
					<Day>28</Day>
				</PubDate>
			</History>
		<Abstract>Colorectal cancer (CRC) remains a major global health concern, especially given its increasing incidence among younger individuals. While genome-wide association studies (GWAS) have identified numerous CRC-associated polymorphisms, their spatial distribution and functional implications are not fully understood. This study examined the locations of 1,346 CRC-linked polymorphisms across chromosomal bands. The results revealed significant nonrandom clustering across thirteen chromosomal bands: 1q41, 6p21, 8q24, 9q34, 10p14, 10q25, 11q12, 12p13, 15q13, 18q21, 19q13, 20p12, and 20q13. Functional enrichment analysis of genes within these bands revealed several Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Reciprocal chromosomal enrichment confirmed that many of these terms and pathways were not randomly localized within the same bands, highlighting their potential biological significance. Survival analysis using TCGA data identified three KEGG pathways and 33 GO terms mapped to nine of the thirteen bands that were significantly associated with poor prognosis. Notably, the 8q24 and 20q13 regions were enriched for differentially expressed genes and survival-associated terms yet showed no significant enrichment for genes with high somatic mutation rates. These results imply that 8q24 and 20q13 act as regulatory hotspots rather than mutation-driven regions. Overall, this integrative approach identified functionally and clinically relevant genomic regions that may contribute to inherited CRC risk and progression, providing valuable targets for the development of diagnostic and prognostic biomarkers.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Chromosomal Bands</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Colorectal cancer</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Enrichment Analysis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Genome-Wide Association Studies</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Polymorphism</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8296_3e311499954b7347abe29e657b77b848.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>CPUK02 sensitizes U87 glioblastoma cell lines to TMZ treatment via autophagy flux inhibition</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>11</FirstPage>
			<LastPage>20</LastPage>
			<ELocationID EIdType="pii">8298</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.52011.2079</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Hooman</FirstName>
					<LastName>Rezaie</LastName>
<Affiliation>Department of Clinical Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Sanaz</FirstName>
					<LastName>Dastghaib</LastName>
<Affiliation>Endocrinology and Metabolism Research Center, Shiraz University of Medical Science, Shiraz, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Morvarid</FirstName>
					<LastName>Siri</LastName>
<Affiliation>Autophagy Research center, Shiraz University of Medical Sciences, Shiraz, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Pooneh</FirstName>
					<LastName>Mokarram</LastName>
<Affiliation>Autophagy Research Center, Department of Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Mina</FirstName>
					<LastName>Hemmati</LastName>
<Affiliation>Department of Clinical Biochemistry, School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2024</Year>
					<Month>12</Month>
					<Day>25</Day>
				</PubDate>
			</History>
		<Abstract>Adjuvant chemotherapy with TMZ (Temozolomide) does not improve the survival of patients suffering from GBM (Glioblastoma). Given the importance of autophagy and UPR (Unfolding Protein Response) in chemotherapy resistance, as well as the role of &lt;em&gt;Beclin-1, LC3IIβ&lt;/em&gt;, and &lt;em&gt;P62&lt;/em&gt; in the regulation of autophagy, we evaluated the effect of TMZ along with CPUK02 on U87 cells as a model of Glioblastoma cancer in this study. To achieve this goal, we treated the U87 cells with different doses of TMZ (50, 100, 200, 400, and 800 μM) and CPUK02 (1, 0.5, 0.25, 0.125, 0.06, 0.03, 0.01, and 0.007 μM); then, cell viability was assessed by MTT assay.  The gene expression of &lt;em&gt;Beclin1, P62, LC3IIβ,&lt;/em&gt; and &lt;em&gt;XBP-1s&lt;/em&gt; was analyzed using quantitative real-time polymerase chain reaction. The comparison of the control group with the groups treated with the TMZ drug showed that, in 48 and 72 hours, doses of TMZ more than IC&lt;sub&gt;50&lt;/sub&gt; (100 μM) (&lt;em&gt;p&lt;/em&gt;&lt;0.001) significantly led to cell death. CPUK02 doses more than 0.125 (&lt;em&gt;p&lt;/em&gt;&lt;0.0001) significantly led to cell death. TMZ and CPUK02 combination therapy (100 and 0.03 μM, respectively) increased the expression of &lt;em&gt;Beclin-1, LC3IIβ&lt;/em&gt;, and &lt;em&gt;P62&lt;/em&gt; and  activated the IRE-1 arm of UPR by increasing the expression of XBP-1s. TMZ and CPUK02 treatment inhibits the autophagic flux (&lt;em&gt;p62, LC3IIβ&lt;/em&gt;).&lt;strong&gt;&lt;em&gt; &lt;/em&gt;&lt;/strong&gt;Increased &lt;em&gt;XBP-1s&lt;/em&gt; expression might contribute to the enhanced TMZ sensitivity. This combination therapy is promising for TMZ-resistant cancers, but it needs further investigation.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">CPUK02</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">TMZ</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Autophagy</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Glioblastoma</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">UPR</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8298_e13a2880fa3023f4a8b56d436d46d270.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Analysis of amino acid residues affecting the transcriptional activity of nuclear factor Ya</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>21</FirstPage>
			<LastPage>29</LastPage>
			<ELocationID EIdType="pii">8301</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.54185.2206</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Duhan</FirstName>
					<LastName>Tao</LastName>

						<AffiliationInfo>
						<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Nutrigenomics Research Group, Institute of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Yoshinori</FirstName>
					<LastName>Takeuchi</LastName>
<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Samia</FirstName>
					<LastName>Karkoutly</LastName>
<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Zahra</FirstName>
					<LastName>Mehrazad Saber</LastName>
<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Ye</FirstName>
					<LastName>Chen</LastName>

						<AffiliationInfo>
						<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Nutrigenomics Research Group, Institute of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Tsolmon</FirstName>
					<LastName>Mendsaikhan</LastName>
<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Rika</FirstName>
					<LastName>Saikawa</LastName>
<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Yuichi</FirstName>
					<LastName>Aita</LastName>

						<AffiliationInfo>
						<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Nutrigenomics Research Group, Institute of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Yuki</FirstName>
					<LastName>Murayama</LastName>
<Affiliation>Nutrigenomics Research Group, Institute of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Akito</FirstName>
					<LastName>Shikama</LastName>
<Affiliation>Nutrigenomics Research Group, Institute of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Yukari</FirstName>
					<LastName>Masuda</LastName>
<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>

</Author>
<Author>
					<FirstName>Naoya</FirstName>
					<LastName>Yahagi</LastName>

						<AffiliationInfo>
						<Affiliation>Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical University, Tochigi 329-0498, Japan</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Nutrigenomics Research Group, Institute of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan</Affiliation>
						</AffiliationInfo>
<Identifier Source="ORCID">0000-0002-1823-1865</Identifier>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>09</Month>
					<Day>05</Day>
				</PubDate>
			</History>
		<Abstract>Nuclear factor Y (NF-Y) is a heterotrimeric transcription factor essential for regulating genes involved in lipid metabolism, including fatty acid synthase (Fasn). Although NF-Y activity is known to be dynamically regulated during adipocyte differentiation, the amino acid residues responsible for its transcriptional function remain unclear. In this study, we examined the contribution of nuclear factor Ya (NF-Ya) to DNA-binding activity and transcriptional regulation in 3T3-L1 adipocytes. Using deletion constructs and adenoviral expression systems, we identified a region spanning amino acid residues 184-347 of NF-Ya as critical for acquiring DNA-binding ability during differentiation. Electrophoretic mobility shift assays revealed that NF-Ya undergoes modification within this region, conferring stage-specific DNA-binding activity to the &lt;em&gt;Fasn&lt;/em&gt; promoter. These findings suggest that post-translational modification of NF-Ya is a key mechanism regulating NF-Y function in adipogenesis. Our work provides novel insights into transcriptional control of lipogenic genes and their relevance to metabolic regulation.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Adipogenesis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Fatty acid synthesis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">transcription</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8301_0a82367c32b78aa446c7bc9953906735.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Wharton's jelly mesenchymal stem cell-derived conditioned media inhibits colon cancer cells via activating AMPK/mTOR-mediated autophagy</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>31</FirstPage>
			<LastPage>38</LastPage>
			<ELocationID EIdType="pii">8302</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.52891.2133</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Dian</FirstName>
					<LastName>Dayer</LastName>
<Affiliation>Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Zahra</FirstName>
					<LastName>Akbari-Jonoush</LastName>

						<AffiliationInfo>
						<Affiliation>Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Department of Immunology, School of Medicine Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Roya</FirstName>
					<LastName>Mahdavi</LastName>

						<AffiliationInfo>
						<Affiliation>Department of Immunology, School of Medicine Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Afshin</FirstName>
					<LastName>Amari</LastName>

						<AffiliationInfo>
						<Affiliation>Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Department of Immunology, School of Medicine Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Amirhesam</FirstName>
					<LastName>Keshavarz-Zarjani</LastName>

						<AffiliationInfo>
						<Affiliation>Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Layasadat</FirstName>
					<LastName>Khorsandi</LastName>

						<AffiliationInfo>
						<Affiliation>Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran</Affiliation>
						</AffiliationInfo>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>04</Month>
					<Day>09</Day>
				</PubDate>
			</History>
		<Abstract>Prior studies have shown that conditioned media derived from Wharton&#039;s jelly mesenchymal stem cells (WJ-CM) have anti-cancer properties. This research investigated the impact of WJ-CM on HT-29 colorectal adenocarcinoma cells by examining autophagy biomarkers and the AMPK/mTOR pathway. The HT-29 cells were subjected to WJ-CM and an AMPK activator (AICAR). Autophagy and levels of AMPK and mTOR proteins were investigated. WJ-CM increased the expression of phosphorylated AMPK while reducing the level of phosphorylated mTOR in HT-29 cells. WJ-CM treatment elevated the LC3B/LC3A ratio and ATG7, ATG5, and Beclin-1 expression. However, there was a parallel drop in p62 expression, which indicates autophagy induction. AICAR increased the influence of WJ-CM on viability, as well as the levels of biomarkers associated with autophagy, phosphorylated  AMPK, and phosphorylated  mTOR in the HT-29 cells. WJ-CM inhibits colorectal cancer cell growth via activating AMPK/mTOR-mediated autophagy.</Abstract>
		<ObjectList>
			<Object Type="keyword">
			<Param Name="value">Colon cancer</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">AMPK</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Stem Cell</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Autophagy</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8302_06f34c393af3b61c8b4db69745e97dca.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Molecular dynamics simulation of thermal activation of human TRPV1</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>39</FirstPage>
			<LastPage>48</LastPage>
			<ELocationID EIdType="pii">8332</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.53301.2171</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Juan David</FirstName>
					<LastName>Bermudes-Contreras</LastName>
<Affiliation>Sección de Estudios de Posgrado e Investigación, Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Ciudad de México, México</Affiliation>

</Author>
<Author>
					<FirstName>Luis Manuel</FirstName>
					<LastName>Arratia-Cortés</LastName>
<Affiliation>Sección de Estudios de Posgrado e Investigación, Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Ciudad de México, México</Affiliation>

</Author>
<Author>
					<FirstName>María Esther</FirstName>
					<LastName>Ramírez-Moreno</LastName>
<Affiliation>Sección de Estudios de Posgrado e Investigación, Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Ciudad de México, México</Affiliation>

</Author>
<Author>
					<FirstName>Beatriz</FirstName>
					<LastName>Zamora-López</LastName>
<Affiliation>Departamento de Psiquiatría y Salud Mental, Facultad de Medicina, UNAM, Ciudad de México, México</Affiliation>

</Author>
<Author>
					<FirstName>César</FirstName>
					<LastName>López-Camarillo</LastName>
<Affiliation>Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Ciudad de México, México</Affiliation>

</Author>
<Author>
					<FirstName>Laurence Annie</FirstName>
					<LastName>Marchat</LastName>
<Affiliation>Sección de Estudios de Posgrado e Investigación, Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Ciudad de México, México</Affiliation>

</Author>
<Author>
					<FirstName>Absalom</FirstName>
					<LastName>Zamorano-Carrillo</LastName>
<Affiliation>Sección de Estudios de Posgrado e Investigación, Escuela Nacional de Medicina y Homeopatía, Instituto Politécnico Nacional, Ciudad de México, México</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>06</Month>
					<Day>03</Day>
				</PubDate>
			</History>
		<Abstract>TRPV1 (Transient Receptor Potential Vanilloid 1) is a non-selective ion channel that responds to various thermal, chemical, mechanical, and ligand stimuli. It is expressed in various tissues, mainly in nociceptive neurons, adipocytes, and other cell types. This channel is involved in pain and temperature transition processes, although it has recently been implicated in adipocyte browning processes. That is why the study of this receptor has increased in recent years to understand the process of activation and inactivation by various stimuli. In this work, we focus on modeling a complete channel of human TRPV1 (hTRPV1), the structural changes, and especially the behavior of the pore when this protein is subjected to high temperatures (400 K). We report that when molecular dynamics simulate hTRPV1 at 400 K, it suffers an increase in the diameter of the two gates reported elsewhere in the pore, suggesting the opening of the channel. In this work, we describe the structural changes in the entire protein, concomitant to those in the pore, favoring this process, which might be associated with its biological activity.</Abstract>
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			<Param Name="value">TRPV1 channel</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Heat activation</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">molecular dynamics</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Pore</Param>
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		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8332_22c6dada8fab333e167ea93f13389fca.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Integrative computational approach to farnesyltransferase inhibition toward anti-liver cancer drug candidate from Syzygium cumini essential oils</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>49</FirstPage>
			<LastPage>61</LastPage>
			<ELocationID EIdType="pii">8333</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.54110.2201</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Wira Eka</FirstName>
					<LastName>Putra</LastName>
<Affiliation>Biotechnology Study Program, Department of Applied Sciences, Faculty of Mathematics and Natural Sciences, Universitas Negeri Malang, East Java, 65145, Indonesia</Affiliation>

</Author>
<Author>
					<FirstName>Arief</FirstName>
					<LastName>Hidayatullah</LastName>
<Affiliation>Democratic Governance and Poverty Reduction Unit, United Nations Development Programme, Eijkman-RSCM Building, Jakarta, 10430, Indonesia</Affiliation>

</Author>
<Author>
					<FirstName>Diana</FirstName>
					<LastName>Widiastuti</LastName>
<Affiliation>Department of Chemistry, Faculty of Mathematics and Natural Science, Universitas Pakuan, West Java, 16129, Indonesia</Affiliation>

</Author>
<Author>
					<FirstName>Hary</FirstName>
					<LastName>Isnanto</LastName>
<Affiliation>Department of Biochemical Technology, School of Bioresources and Technology, King Mongkut's University of Technology Thonburi, Bangkok, 10140, Thailand</Affiliation>

</Author>
<Author>
					<FirstName>Muhammad</FirstName>
					<LastName>Fikri Heikal</LastName>
<Affiliation>Tropical Medicine Graduate Program, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand</Affiliation>

</Author>
<Author>
					<FirstName>S</FirstName>
					<LastName>Sustiprijatno</LastName>
<Affiliation>Research Center for Applied Botany, National Research and Innovation Agency, West Java, 16911, Indonesia</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>08</Month>
					<Day>28</Day>
				</PubDate>
			</History>
		<Abstract>Farnesyltransferase plays a critical role in the post-translational modification of mammalian proteins, including the Ras oncogene, which is strongly associated with cancer development. Essential oils from &lt;em&gt;Syzygium cumini&lt;/em&gt; have demonstrated promising therapeutic effects, particularly in cancer treatment, potentially through the inhibition of farnesyltransferase activity. This study employed integrative computational approaches to investigate the anticancer potential of essential oils derived from &lt;em&gt;S. cumini&lt;/em&gt;. Various compounds were screened for toxicity, biological activities, membrane permeability, gene expression profiles, and survival correlations were conducted to investigate cancer-associated properties. Molecular docking and molecular dynamics (MD) simulations were performed to evaluate the binding interactions and stability of ligand–protein complexes involving farnesyltransferase. α-Humulene epoxide II exhibited antineoplastic activity, functioned as an apoptosis agonist, and inhibited cancer-related targets such as HIF1A and MMP9. Bornyl acetate showed potential as a JAK2 inhibitor. Both compounds demonstrated favorable membrane permeability, indicating high bioavailability and effective cellular uptake. Analysis of the farnesyltransferase (FNTB) gene revealed significantly higher expression in cancerous tissues and a positive correlation with pro-tumor immune cell infiltration. Molecular docking identified Tipifarnib as the strongest binder, serving as a positive control, while α-humulene epoxide II and bornyl acetate showed moderate to weaker binding affinities. However, MD simulations confirmed that both essential oil compounds exhibit binding stability comparable to that of Tipifarnib. Finally, α-humulene epoxide II and bornyl acetate from &lt;em&gt;S. cumini&lt;/em&gt; exhibit favorable drug-like properties, high predicted safety margins, and a lack of organ-specific toxicity, underscoring their suitability for further drug development.</Abstract>
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			<Param Name="value">In silico</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Metastasis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">MMP9</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Natural Products</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">S. cumini</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8333_12243f79b6cd9661ccab4c82f546f015.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Prediction of microRNAs affecting the syncytin-1 (HERV-W) and syncytin-2 (HERV-FRD) genes regulation in endometriosis and miscarriage</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>63</FirstPage>
			<LastPage>70</LastPage>
			<ELocationID EIdType="pii">8370</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.54457.2225</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Mehdi</FirstName>
					<LastName>Gholami-Barzoki</LastName>
<Affiliation>Department of Virology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Somayeh</FirstName>
					<LastName>Shatizadeh-Malekshahi</LastName>
<Affiliation>Department of Virology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Mohammad</FirstName>
					<LastName>Shayestehpour</LastName>
<Affiliation>Department of Bacteriology and Virology, Faculty of  Medicine, Isfahan University of Medical Sciences, Isfahan, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Haleh</FirstName>
					<LastName>Soltanghoraee</LastName>
<Affiliation>Reproductive Biotechnology Research Center, Avicenna Research Institute, ACECR, Tehran, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>10</Month>
					<Day>04</Day>
				</PubDate>
			</History>
		<Abstract>Abnormal expression levels of microRNAs are associated with numerous diseases in the female reproductive tract. A small subset of human endogenous retroviruses (HERVs) genes have retained open reading frames (ORFs) that serve beneficial functions for the host. Syncytin-1 (HERV-W) and Syncytin-2 (HERV-FRD) play crucial roles in mammalian development and are expressed in placental trophoblasts. The miRNAs associated with HERV-W and HERV-FRD in spontaneous abortion and endometriosis have not been elucidated. The present study aimed to identify potential miRNAs that affect the regulation of Syncytin-1 and Syncytin-2 in endometriosis and miscarriage using bioinformatics tools. Complete CDS of Syncytin-1 (ERVW-1) and Syncytin-2 (ERVFRD-1) genes were collected from the gene bank database. Several target prediction algorithms were utilized, such as TargetScan, DIANA, miRDB, and miRWalk. Complete CDS of Syncytin-1 (ERVW-1) and Syncytin-2 (ERVFRD-1) genes were collected from the gene bank database. By integrating data from these diverse bioinformatics databases, miR-509-3p and miR-625-5p were consistent across multiple platforms, ensuring robust selection criteria. These tools facilitate the identification of differentially expressed miRNAs, understanding their roles in cellular processes, and potentially utilizing them as biomarkers for disease diagnosis and prognosis. Validation of the identified miRNAs in experimental models or clinical samples is needed to confirm their roles in endometriosis and miscarriage. </Abstract>
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			<Object Type="keyword">
			<Param Name="value">MicroRNA</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Endometriosis</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Miscarriage</Param>
			</Object>
			<Object Type="keyword">
			<Param Name="value">Human endogenous retroviruses</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8370_de6a03e3adcdaad82227b8cea15fe256.pdf</ArchiveCopySource>
</Article>

<Article>
<Journal>
				<PublisherName>Shiraz University Press</PublisherName>
				<JournalTitle>Molecular Biology Research Communications</JournalTitle>
				<Issn>2322-181X</Issn>
				<Volume>15</Volume>
				<Issue>1</Issue>
				<PubDate PubStatus="epublish">
					<Year>2026</Year>
					<Month>03</Month>
					<Day>01</Day>
				</PubDate>
			</Journal>
<ArticleTitle>Genetic polymorphisms of GSTM1 and GSTT1 genes: effects on susceptibility to formaldehyde-induced hematotoxicity</ArticleTitle>
<VernacularTitle></VernacularTitle>
			<FirstPage>71</FirstPage>
			<LastPage>79</LastPage>
			<ELocationID EIdType="pii">8371</ELocationID>
			
<ELocationID EIdType="doi">10.22099/mbrc.2025.54313.2213</ELocationID>
			
			<Language>EN</Language>
<AuthorList>
<Author>
					<FirstName>Reza</FirstName>
					<LastName>Pourbabaki</LastName>

						<AffiliationInfo>
						<Affiliation>Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran</Affiliation>
						</AffiliationInfo>

						<AffiliationInfo>
						<Affiliation>Department of Occupational Health and Safety Engineering, Shiraz University of Medical Sciences, Shiraz, Iran</Affiliation>
						</AffiliationInfo>

</Author>
<Author>
					<FirstName>Seyed Ahmadreza</FirstName>
					<LastName>Siadat</LastName>
<Affiliation>Department of Biology, School of Science, Shiraz University, Shiraz, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Saeed</FirstName>
					<LastName>Yousefinejad</LastName>
<Affiliation>Department of Occupational Health and Safety Engineering, Shiraz University of Medical Sciences, Shiraz, Iran</Affiliation>

</Author>
<Author>
					<FirstName>Esmaeel</FirstName>
					<LastName>Soleimani</LastName>
<Affiliation>Department of Occupational Health and Safety Engineering, Shiraz University of Medical Sciences, Shiraz, Iran</Affiliation>

</Author>
</AuthorList>
				<PublicationType>Journal Article</PublicationType>
			<History>
				<PubDate PubStatus="received">
					<Year>2025</Year>
					<Month>09</Month>
					<Day>19</Day>
				</PubDate>
			</History>
		<Abstract>Formaldehyde (FA) is a known human carcinogen for the upper respiratory tract. However, its hematotoxicity remains unclear. This study was performed to assess probable effects of FA on blood parameters and to determine the common polymorphisms in the detoxification enzymes &lt;em&gt;GSTM1&lt;/em&gt; and &lt;em&gt;GSTT1&lt;/em&gt; as biomarkers of susceptibility. Sixty-four workers with high occupational FA exposure and 57 non-exposed controls were studied. Complete blood count was performed. Also, &lt;em&gt;GSTM1&lt;/em&gt;/&lt;em&gt;GSTT1&lt;/em&gt; genotypes were determined. After adjusting for potential confounding variables, FA exposure was only associated with the levels of hemoglobin, mean corpuscular hemoglobin concentration, and reticulocytes. Notably, workers with homozygous deletions of &lt;em&gt;GSTM1&lt;/em&gt; or &lt;em&gt;GSTT1&lt;/em&gt; had hematological parameters similar to those with active genes. In conclusion, very high FA exposure resulted in only slight alterations in MCHC and no overt hematotoxicity was observed. These findings suggest that even at high exposure levels, FA may not reach the bone marrow in sufficient amounts to cause hematotoxicity. Also, it seems that &lt;em&gt;GSTM1&lt;/em&gt;/&lt;em&gt;GSTT1&lt;/em&gt; polymorphisms do not influence the workers’ susceptibility to FA-related blood effects.</Abstract>
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			<Param Name="value">Formaldehyde</Param>
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			<Object Type="keyword">
			<Param Name="value">Hematotoxicity</Param>
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			<Object Type="keyword">
			<Param Name="value">Genetic polymorphism</Param>
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			<Object Type="keyword">
			<Param Name="value">Occupational exposure</Param>
			</Object>
		</ObjectList>
<ArchiveCopySource DocType="pdf">https://mbrc.shirazu.ac.ir/article_8371_ff9c9212102b1c74058aa44d38312d69.pdf</ArchiveCopySource>
</Article>
</ArticleSet>
