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Article: Expression Profiles of Hepatic Immune Response Genes in HEV Infection.

Badshah, Yasmin / Shabbir, Maria / Khan, Khushbukhat / Akhtar, Hashaam

2023 Volume 12, Issue 3

Abstract: Hepatitis E is a liver inflammation caused by infection with the hepatitis E virus (HEV). Every year, there are an estimated 20 million HEV infections worldwide, leading to an estimated 3.3 million symptomatic cases of hepatitis E. HEV viral load has ... ...

Abstract	Hepatitis E is a liver inflammation caused by infection with the hepatitis E virus (HEV). Every year, there are an estimated 20 million HEV infections worldwide, leading to an estimated 3.3 million symptomatic cases of hepatitis E. HEV viral load has been studied about the disease progression; however, hepatic the host gene expression against HEV infection remains unknown.
Language	English
Publishing date	2023-03-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens12030392
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Article ; Online: Impact of deleterious missense PRKCI variants on structural and functional dynamics of protein.

Shah, Hania / Khan, Khushbukhat / Khan, Naila / Badshah, Yasmin / Ashraf, Naeem Mahmood / Shabbir, Maria

Scientific reports

2022 Volume 12, Issue 1, Page(s) 3781

Abstract: Protein kinase C iota ( ... ...

Abstract	Protein kinase C iota (PKC
MeSH term(s)	Isoenzymes ; Mutation, Missense ; Polymorphism, Single Nucleotide ; Protein Kinase C/genetics ; Proteins/genetics
Chemical Substances	Isoenzymes ; Proteins ; Protein Kinase C (EC 2.7.11.13) ; protein kinase C lambda (EC 2.7.11.13)
Language	English
Publishing date	2022-03-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-07526-4
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Article ; Online: Manipulation of Interleukin-6 (IL-6) and Transforming Growth Factor Beta-1(TGFβ-1) towards viral induced liver cancer pathogenesis.

Badshah, Yasmin / Shabbir, Maria / Khan, Khushbukhat / Fatima, Maha / Majoka, Iqra / Aslam, Laiba / Munawar, Huda

PloS one

2022 Volume 17, Issue 10, Page(s) e0275834

Abstract: Hepatocellular carcinoma (HCC) is the most common liver malignancy. Early diagnosis of HCC has always been challenging. This study aims to assess the pathogenicity and the prevalence of IL-6 -174G/C (rs1800795) and TGFβ-1 +29C/T (rs1800470) polymorphisms ...

Abstract	Hepatocellular carcinoma (HCC) is the most common liver malignancy. Early diagnosis of HCC has always been challenging. This study aims to assess the pathogenicity and the prevalence of IL-6 -174G/C (rs1800795) and TGFβ-1 +29C/T (rs1800470) polymorphisms in HCV-infected HCC patients. Experimental strategies are integrated with computational approaches to analyse the pathogenicity of the TGFβ-1 +29C/T and IL-6-174 G/C polymorphisms in HCV-induced HCC. AliBaba2 was used to predict the effect of IL-6-174 G/C on transcription factor binding site in IL-6 gene. Structural changes in the mutant TGFβ-1 structure were determined through project HOPE. To assess the polymorphic prevalence of IL-6 -174G/C and TGFβ-1 +29C/T genotypes in HCC and control subjects, amplification refractory mutation system PCR (ARMS-PCR) was performed on 213 HCC and 216 control samples. GraphPad Prism version 8.0 was used for the statistical analysis of the results. In-silico analysis revealed the regulatory nature of both IL-6 -174G/C and TGFβ-1 +29C/T polymorphisms. ARMS-PCR results revealed that the individuals carrying TT genotype for TGFβ-1 gene have an increased risk of developing HCC (p<0.0001, OR = 5.403, RR = 2.062) as compared to individuals with CT and CC genotype. Similarly, GC genotype carriers for IL-6 gene exhibit an increased risk of HCC susceptibility (p<0.0001, OR = 2.276, RR = 1.512) as compared to the people carrying the GG genotype. Genotype TT of TGFβ-1 gene and genotype GC of IL-6 gene are found to be associated with HCV-induced HCC. IL-6 polymorphism may alter its transcription that leads to its pathogenicity. TGFβ-1 polymorphism may alter protein structure stability.
MeSH term(s)	Alleles ; Carcinoma, Hepatocellular/pathology ; Carcinoma, Hepatocellular/virology ; Case-Control Studies ; Genetic Predisposition to Disease ; Genotype ; Hepatitis C/complications ; Hepatitis C/genetics ; Humans ; Interleukin-6/genetics ; Liver Neoplasms/pathology ; Liver Neoplasms/virology ; Polymorphism, Single Nucleotide ; Transcription Factors/genetics ; Transforming Growth Factor beta1/genetics
Chemical Substances	IL6 protein, human ; Interleukin-6 ; TGFB1 protein, human ; Transcription Factors ; Transforming Growth Factor beta1
Language	English
Publishing date	2022-10-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0275834
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Article ; Online: Influence of PRKCE non-synonymous variants on protein dynamics and functionality.

Khan, Khushbukhat / Shah, Hania / Rehman, Areeba / Badshah, Yasmin / Ashraf, Naeem M / Shabbir, Maria

Human molecular genetics

2022 Volume 31, Issue 13, Page(s) 2236–2261

Abstract: Novel protein kinase C (nPKC) family member, protein kinase C epsilon (PKCε) is an AGC kinase superfamily member. It is associated with neurological and metabolic diseases as well as human cancers. No study so far has been conducted to identify genetic ... ...

Abstract	Novel protein kinase C (nPKC) family member, protein kinase C epsilon (PKCε) is an AGC kinase superfamily member. It is associated with neurological and metabolic diseases as well as human cancers. No study so far has been conducted to identify genetic variations and their effect on PKCε folding and functioning. The present study aimed to identify mutational hotspots in PKCε and disease-causing non-synonymous variants (nsSNPs) along with the investigation of nsSNP impact on protein dynamics. Twenty-nine in silico tools were applied to determine nsSNP deleteriousness, their impact on protein dynamics and disease association, along with the prediction of PKCε post-translational modification (PTM) sites. The present study's outcomes indicated that most nsSNPs were concentrated in the PKCε hinge region and C-terminal tail. Most pathogenic variants mapped to the kinase domain. Regulatory domain variants influenced PKCε interaction with molecular players whereas kinase domain variants were predicted to impact its phosphorylation pattern and protein-protein interactions. Most PTM sites were mapped to the hinge region. PKCε nsSNPs have an association with oncogenicity and its expression dysregulation is responsible for poor overall survival. Understanding nsSNP structural impact is a primary step necessary for delineating the relationship of genetic level differences with protein phenotype. The obtained knowledge can eventually help in disease diagnosis and therapy design.
MeSH term(s)	Mutation ; Phenotype ; Phosphorylation ; Protein Kinase C-epsilon/genetics ; Protein Kinase C-epsilon/metabolism ; Proteins/genetics
Chemical Substances	Proteins ; Protein Kinase C-epsilon (EC 2.7.11.13)
Language	English
Publishing date	2022-02-08
Publishing country	England
Document type	Journal Article
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddac029
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Article ; Online: Investigation of UTR Variants by Computational Approaches Reveal Their Functional Significance in

Shah, Hania / Khan, Khushbukhat / Badshah, Yasmin / Mahmood Ashraf, Naeem / Shabbir, Maria / Trembley, Janeen H / Afsar, Tayyaba / Abusharha, Ali / Razak, Suhail

Genes

2023 Volume 14, Issue 2

Abstract: Single nucleotide polymorphisms (SNPs) are associated with many diseases including neurological disorders, heart diseases, diabetes, and different types of cancers. In the context of cancer, the variations within non-coding regions, including UTRs, have ... ...

Abstract	Single nucleotide polymorphisms (SNPs) are associated with many diseases including neurological disorders, heart diseases, diabetes, and different types of cancers. In the context of cancer, the variations within non-coding regions, including UTRs, have gained utmost importance. In gene expression, translational regulation is as important as transcriptional regulation for the normal functioning of cells; modification in normal functions can be associated with the pathophysiology of many diseases. UTR-localized SNPs in the PRKCI gene were evaluated using the PolymiRTS, miRNASNP, and MicroSNIper for association with miRNAs. Furthermore, the SNPs were subjected to analysis using GTEx, RNAfold, and PROMO. The genetic intolerance to functional variation was checked through GeneCards. Out of 713 SNPs, a total of thirty-one UTR SNPs (three in 3' UTR region and twenty-nine in 5' UTR region) were marked as ≤2b by RegulomeDB. The associations of 23 SNPs with miRNAs were found. Two SNPs, rs140672226 and rs2650220, were significantly linked with expression in the stomach and esophagus mucosa. The 3' UTR SNPs rs1447651774 and rs115170199 and the 5' UTR region variants rs778557075, rs968409340, and 750297755 were predicted to destabilize the mRNA structure with substantial change in free energy (∆G). Seventeen variants were predicted to have linkage disequilibrium with various diseases. The SNP rs542458816 in 5' UTR was predicted to put maximum influence on transcription factor binding sites. Gene damage index(GDI) and loss of function (o:e) ratio values for PRKCI suggested that the gene is not tolerant to loss of function variants. Our results highlight the effects of 3' and 5' UTR SNP on miRNA, transcription and translation of PRKCI. These analyses suggest that these SNPs can have substantial functional importance in the PRKCI gene. Future experimental validation could provide further basis for the diagnosis and therapeutics of various diseases.
MeSH term(s)	Humans ; 3' Untranslated Regions ; 5' Untranslated Regions ; Gene Expression Regulation ; MicroRNAs/genetics ; Neoplasms/genetics ; Polymorphism, Single Nucleotide ; Protein Kinase C/genetics
Chemical Substances	3' Untranslated Regions ; 5' Untranslated Regions ; MicroRNAs ; protein kinase C lambda (EC 2.7.11.13) ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2023-01-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14020247
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Article: Non-synonymous SNPs variants of PRKCG and its association with oncogenes predispose to hepatocellular carcinoma.

Abid, Fizzah / Khan, Khushbukhat / Badshah, Yasmin / Ashraf, Naeem Mahmood / Shabbir, Maria / Hamid, Arslan / Afsar, Tayyaba / Almajwal, Ali / Razak, Suhail

Cancer cell international

2023 Volume 23, Issue 1, Page(s) 123

Abstract: Background: PRKCG encodes PKC γ, which is categorized under the classical protein kinase C family. No studies have specifically established the relationship between PRKCG nsSNPs with structural and functional variations in PKC γ in the context of ... ...

Abstract	Background: PRKCG encodes PKC γ, which is categorized under the classical protein kinase C family. No studies have specifically established the relationship between PRKCG nsSNPs with structural and functional variations in PKC γ in the context of hepatocellular carcinoma (HCC). The present study aims to uncover this link through in-silico and experimental studies. Methods: The 3D structure of PKC γ was predicted. Molecular Dynamic (MD) Simulations were run and estimates were made for interactions, stability, conservation and post-translational alterations between wild and mutant structures. The association of PRKCG levels with HCC survival rate was determined. Genotyping analyses were conducted to investigate the deleterious PRKCG nsSNP association with HCC. mRNA expression of PKC γ, HIF-1 alpha, AKT, SOCS3 and VEGF in the blood of controls and HCC patients was analyzed and a genetic cascade was constructed depicting these interactions. Results: The expression level of studied oncogenes was compared to tumour suppressor genes. Through Alphafold, the 3D structure of PKC γ was explored. Fifteen SNPs were narrowed down for in-silico analyses that were identified in exons 5, 10 and 18 and the regulatory and kinase domain of PKC γ. Root mean square deviation and fluctuation along with the radius of gyration unveiled potential changes between the wild and mutated variant structures. Mutant genotype AA (homozygous) corresponding to nsSNP, rs386134171 had more frequency in patients with OR (2.446), RR (1.564) and P-values (< 0.0029) that highlights its significant association with HCC compared to controls in which the wild genotype GG was found more prevalent. Conclusion: nsSNP rs386134171 can be a genetic marker for HCC diagnosis and therapeutic studies. This study has laid down a road map for future studies to be conducted on HCC.
Language	English
Publishing date	2023-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-023-02965-z
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Article: Possible prognostic impact of PKCι genetic variants in prostate cancer.

Hafeez, Amna / Shabbir, Maria / Khan, Khushbukhat / Trembley, Janeen H / Badshah, Yasmin / Zafar, Sameen / Shahid, Kanza / Shah, Hania / Ashraf, Naeem Mahmood / Hamid, Arslan / Afsar, Tayyaba / Almajwal, Ali / Marium, Afifa / Razak, Suhail

Cancer cell international

2024 Volume 24, Issue 1, Page(s) 24

Abstract: Background: Single nucleotide polymorphisms (SNPs) have been linked with prostate cancer (PCa) and have shown potential as prognostic markers for advanced stages. Loss of function mutations in PKCι have been linked with increased risk of malignancy by ... ...

Abstract	Background: Single nucleotide polymorphisms (SNPs) have been linked with prostate cancer (PCa) and have shown potential as prognostic markers for advanced stages. Loss of function mutations in PKCι have been linked with increased risk of malignancy by enhancing tumor cell motility and invasion. We have evaluated the impact of two coding region SNPs on the PKCι gene (PRKCI) and their prognostic potential. Methods: Genotypic association of non-synonymous PKCι SNPs rs1197750201 and rs1199520604 with PCa was determined through tetra-ARMS PCR. PKCι was docked with interacting partner Par-6 to determine the effect of these variants on PKCι binding capabilities. Molecular dynamic simulations of PKCι docked with Par-6 were performed to determine variant effects on PKCι protein interactions. The possible impact of changes in PKCι protein interactions on epithelial cell polarity was hypothesized. Results: PKCι rs1199520604 mutant genotype TT showed association with PCa (p = 0.0055), while rs1197750201 mutant genotype AA also showed significant association with PCa (P = 0.0006). The binding interaction of PKCι with Par-6 was altered for both variants, with changes in Van der Waals energy and electrostatic energy of docked structures. Conclusion: Genotypic analysis of two non-synonymous PKCι variants in association with PCa prognosis was performed. Both variants in the PB1 domain showed potential as a prognostic marker for PCa. In silico analysis of the effect of the variants on PKCι protein interactions indicated they may be involved in PCa progression through aberration of epithelial cell polarity pathways.
Language	English
Publishing date	2024-01-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-023-03182-4
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Article ; Online: Expression of suppressor of cytokine signaling 3 (SOCS3) and interleukin-6 (-174-G/C) polymorphism in atopic conditions.

Jannat, Arooma / Khan, Maryam / Shabbir, Maria / Badshah, Yasmin

PloS one

2019 Volume 14, Issue 6, Page(s) e0219084

Abstract: Hypersensitivity of the immune system is caused by elevated immunoglobulin E (IgE) levels in the serum, in response to a discrete allergen leading to allergic reactions. IgE-mediated inflammation is regulated by the cascade of defense related signaling ... ...

Abstract	Hypersensitivity of the immune system is caused by elevated immunoglobulin E (IgE) levels in the serum, in response to a discrete allergen leading to allergic reactions. IgE-mediated inflammation is regulated by the cascade of defense related signaling molecules including interleukin-6 (IL-6) that plays pivotal role in the survival and maturation of mast cells during an allergic reaction. IL-6 mediated defense responses are tightly regulated by Suppressor of Cytokine Signaling 3 (SOCS3), an inhibitory molecules of Janus Kinase-Signal Transducers and Activators of Transcription (JAK-STAT) signaling, in a negative feedback mechanism. The given study focuses on the assessment of crosstalk between SOCS3 and IL-6 to unravel the molecular significance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. The expression study of SOCS3 through real-time PCR analysis revealed, a 5.9 mean fold increase in SOCS3 expression in atopic cases in comparison to control cases. Moreover, IL-6 has, also, been found significantly enhanced in the serum level of atopic cases (26.4 pg/ml) as compared to control cases (3.686 pg/ml). Female population was found to be at a higher risk to develop atopic condition than male population as females exhibited higher expression of both SOCS3 and IL-6 than males. Furthermore, the polymorphic study of IL-6 promoter region (IL-6 174-G/C) in atopic population has reasserted the importance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. Expression of SOCS3 and IL-6 serum levels were found to be highly correlated. Therefore establishing the role of IL-6 (-174-G/C) polymorphism on the expression of SOCS3 and IL-6 in atopic cases. Notably, the study established SOCS3 and IL-6 as potential targets for the diagnosis/prognosis of allergy and for the development of reliable therapeutic strategies to control atopic conditions in the near future.
MeSH term(s)	Adult ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Humans ; Hypersensitivity/diagnosis ; Hypersensitivity/genetics ; Interleukin-6/genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Sex Factors ; Suppressor of Cytokine Signaling 3 Protein/genetics ; Young Adult
Chemical Substances	Interleukin-6 ; Suppressor of Cytokine Signaling 3 Protein
Language	English
Publishing date	2019-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0219084
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Investigation of UTR Variants by Computational Approaches Reveal Their Functional Significance in PRKCI Gene Regulation

Shah, Hania / Khan, Khushbukhat / Badshah, Yasmin / Mahmood Ashraf, Naeem / Shabbir, Maria / Trembley, Janeen H. / Afsar, Tayyaba / Abusharha, Ali / Razak, Suhail

Genes (Basel). 2023 Jan. 18, v. 14, no. 2

2023

Abstract	Single nucleotide polymorphisms (SNPs) are associated with many diseases including neurological disorders, heart diseases, diabetes, and different types of cancers. In the context of cancer, the variations within non-coding regions, including UTRs, have gained utmost importance. In gene expression, translational regulation is as important as transcriptional regulation for the normal functioning of cells; modification in normal functions can be associated with the pathophysiology of many diseases. UTR-localized SNPs in the PRKCI gene were evaluated using the PolymiRTS, miRNASNP, and MicroSNIper for association with miRNAs. Furthermore, the SNPs were subjected to analysis using GTEx, RNAfold, and PROMO. The genetic intolerance to functional variation was checked through GeneCards. Out of 713 SNPs, a total of thirty-one UTR SNPs (three in 3′ UTR region and twenty-nine in 5′ UTR region) were marked as ≤2b by RegulomeDB. The associations of 23 SNPs with miRNAs were found. Two SNPs, rs140672226 and rs2650220, were significantly linked with expression in the stomach and esophagus mucosa. The 3′ UTR SNPs rs1447651774 and rs115170199 and the 5′ UTR region variants rs778557075, rs968409340, and 750297755 were predicted to destabilize the mRNA structure with substantial change in free energy (∆G). Seventeen variants were predicted to have linkage disequilibrium with various diseases. The SNP rs542458816 in 5′ UTR was predicted to put maximum influence on transcription factor binding sites. Gene damage index(GDI) and loss of function (o:e) ratio values for PRKCI suggested that the gene is not tolerant to loss of function variants. Our results highlight the effects of 3′ and 5′ UTR SNP on miRNA, transcription and translation of PRKCI. These analyses suggest that these SNPs can have substantial functional importance in the PRKCI gene. Future experimental validation could provide further basis for the diagnosis and therapeutics of various diseases.
Keywords	Gibbs free energy ; diabetes ; esophagus ; gene expression ; genes ; heart ; linkage disequilibrium ; microRNA ; mucosa ; pathophysiology ; stomach ; therapeutics ; transcription (genetics) ; transcription factors
Language	English
Dates of publication	2023-0118
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14020247
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Pathogenicity of PKCγ Genetic Variants—Possible Function as a Non-Invasive Diagnostic Biomarker in Ovarian Cancer

Shahid, Kanza / Khan, Khushbukhat / Badshah, Yasmin / Mahmood Ashraf, Naeem / Hamid, Arslan / Trembley, Janeen H. / Shabbir, Maria / Afsar, Tayyaba / Almajwal, Ali / Abusharha, Ali / Razak, Suhail

Genes (Basel). 2023 Jan. 16, v. 14, no. 1

2023

Abstract: Ovarian cancer has the highest mortality rate among gynecologic malignancies, owing to its misdiagnosis or late diagnosis. Identification of its genetic determinants could improve disease outcomes. Conventional Protein Kinase C-γ (PKCγ) dysregulation is ... ...

Abstract	Ovarian cancer has the highest mortality rate among gynecologic malignancies, owing to its misdiagnosis or late diagnosis. Identification of its genetic determinants could improve disease outcomes. Conventional Protein Kinase C-γ (PKCγ) dysregulation is reported in several cancers. Similarly, its variant rs1331262028 is also reported to have an association with hepatocellular carcinoma. Therefore, the aim of the present study was to analyze the variant rs1331262028 association with ovarian cancer and to determine its impact on PKCγ’s protein interactions. Association of variation was determined through genotyping PCR (cohort size:100). Protein–protein docking and molecular dynamic simulation were carried out to study the variant impact of PKCγ interactions. The study outcome indicated the positive association of variant rs1331262028 with ovarian cancer and its clinicopathological features. Molecular dynamics simulation depicted the potential influence of variation on PKCγ molecular signaling. Hence, this study provided the foundations for assessing variant rs1331262028 as a potential prognostic marker for ovarian cancer. Through further validation, it can be applied at the clinical level.
Keywords	biomarkers ; genotyping ; hepatoma ; molecular dynamics ; mortality ; ovarian neoplasms ; pathogenicity ; protein kinases
Language	English
Dates of publication	2023-0116
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14010236
Database	NAL-Catalogue (AGRICOLA)

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