Role of Molecular Markers

2013 ◽  
pp. 165-185 ◽  
Author(s):  
Reyazul Rouf Mir ◽  
Javaid Akhter Bhat ◽  
Nelofer Jan ◽  
Bikram Singh ◽  
Ashok Kumar Razdan ◽  
...  
Keyword(s):  
Molecular Markers

scholarly journals Study of Plant Genetic Variation through Molecular Markers: An Overview

2021 ◽  
pp. 464-473
Author(s):  
Zeina S. M. Al-Hadeithi ◽  
Saade Abdalkareem Jasim
Keyword(s):  
Molecular Markers ◽  
Simple Sequence Repeat Marker ◽  
Fragment Length ◽  
Simple Sequence Repeat ◽  
Plant Biotechnology ◽  
Molecular Techniques ◽  
Basic Material ◽  
Sequence Repeat ◽  
Simple Sequence

This article refers to viewing the role of molecular markers during analyzing the genome of plants and their importance in plant biotechnology. In recent years, we observed the role of molecular techniques in programs for improving plant breeding and preserving genetic resources has been observed, and molecular and biochemical indicators which represent basic material through determining the diversity between genotypes for indicators it is never affected by external surrounding conditions as always in the phenotype features. Molecular markers of DNA have been widely applied to answer a range of questions related to taxonomy, molecular evolution, population genetics, and genetic diversity, as well as monitoring trade in plants and food products , in addition to its having a role in studying gene expression , genetic mapping, and studies of species evolution providing fast and accurate results. In this work, the advantages and limitations of the molecular techniques applied in plant sciences such as: RAPD (Random Amplification Polymorphic DNA Marker); ISSR (Inter Simple Sequence Repeat Marker); SSR (Simple Sequence Repeat Marker); AFLP (Amplified Fragment Length Polymorphic Marker); RFLP (Restriction Fragment Length Polymorphism Marker); SNP (Single Nucleotide Polymorphism) and Real Time PCR.

Role of Proteins as New Molecular Markers for Analyzing Material Structures to Prevent Traumatic Brain Injuries

2021 ◽  
pp. 58-67
Author(s):  
Hans von Holst ◽  
Pasi Purhonen ◽  
Daniel Lanner ◽  
Ramakrishnan Balakrishnan Kumar ◽  
Hans Hebert
Keyword(s):  
Molecular Markers ◽  
Brain Injuries ◽  
Traumatic Brain Injuries

scholarly journals MiR193a Modulation and Podocyte Phenotype

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1004
Author(s):  
Alok Jha ◽  
Shourav Saha ◽  
Kamesh Ayasolla ◽  
Himanshu Vashistha ◽  
Ashwani Malhotra ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Molecular Markers ◽  
Promoter Region ◽  
Therapeutic Strategy ◽  
Protein Complexes ◽  
Md Simulations ◽  
Tertiary Structures ◽  
Docking Approach ◽  
Apolipoprotein L1

Apolipoprotein L1 (APOL1)-miR193a axis has been reported to play a role in the maintenance of podocyte homeostasis. In the present study, we analyzed transcription factors relevant to miR193a in human podocytes and their effects on podocytes’ molecular phenotype. The motif scan of the miR193a gene provided information about transcription factors, including YY1, WT1, Sox2, and VDR-RXR heterodimer, which could potentially bind to the miR193a promoter region to regulate miR193a expression. All structure models of these transcription factors and the tertiary structures of the miR193a promoter region were generated and refined using computational tools. The DNA-protein complexes of the miR193a promoter region and transcription factors were created using a docking approach. To determine the modulatory role of miR193a on APOL1 mRNA, the structural components of APOL1 3’ UTR and miR193a-5p were studied. Molecular Dynamic (MD) simulations validated interactions between miR193a and YY1/WT1/Sox2/VDR/APOL1 3′ UTR region. Undifferentiated podocytes (UPDs) displayed enhanced miR193a, YY1, and Sox2 but attenuated WT1, VDR, and APOL1 expressions, whereas differentiated podocytes (DPDs) exhibited attenuated miR193a, YY1, and Sox2 but increased WT1, VDR, APOL1 expressions. Inhibition of miR193a in UPDs enhanced the expression of APOL1 as well as of podocyte molecular markers; on the other hand, DPD-transfected with miR193a plasmid showed downing of APOL1 as well as podocyte molecular markers suggesting a causal relationship between miR193a and podocyte molecular markers. Silencing of YY1 and Sox2 in UPDs decreased the expression of miR193a but increased the expression of VDR, and CD2AP (a marker of DPDs); in contrast, silencing of WT1 and VDR in DPDs enhanced the expression of miR193a, YY1, and Sox2. Since miR193a-downing by Vitamin D receptor (VDR) agonist not only enhanced the mRNA expression of APOL1 but also of podocyte differentiating markers, suggest that down-regulation of miR193a could be used to enhance the expression of podocyte differentiating markers as a therapeutic strategy.

scholarly journals Role of histopathology and molecular markers in the active surveillance of prostate cancer

2011 ◽  
Vol 50 (sup1) ◽  
pp. 56-60 ◽  
Author(s):  
Rodolfo Montironi ◽  
Lars Egevad ◽  
Anders Bjartell ◽  
Daniel M. Berney
Keyword(s):  
Prostate Cancer ◽  
Molecular Markers ◽  
Active Surveillance

272 LEUKEMIA INHIBITORY FACTOR SIGNALING PATHWAY IN PIG PARTHENOGENETIC PLURIPOTENT CELLS

2009 ◽  
Vol 21 (1) ◽  
pp. 233
Author(s):  
T. A. L. Brevini ◽  
G. Pennarossa ◽  
S. Antonini ◽  
F. Gandolfi
Keyword(s):  
Molecular Markers ◽  
Signaling Pathway ◽  
Leukemia Inhibitory Factor ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Inhibitory Factor ◽  
Germ Layers ◽  
Undifferentiated State ◽  
Undifferentiated Cells

Leukemia inhibitory factor (LIF), its receptor heterodimer (LRβ-gp130), and the related signal transducer and activator of transcription-3 (STAT3) constitute a system controlling self-renewal and pluripotency of embryonic stem cells (ESC) in the mouse, where LIF withdrawal or direct inhibition of STAT3 causes ESC differentiation. By contrast, several studies have demonstrated that LIF is not required to maintain human ESC pluripotency. Scattered information is available in other species, and data on the role of LIF in pig ESC are scanty. The aims of the present study were (a) to characterize the expression profile of gp130, LRβ, and STAT3 in pig parthenogenetic cell lines (ppC), previously derived in our laboratory and shown to be positive for the main pluripotency related markers; (b) to evaluate the role of LIF pathway in maintaining the pluripotency of these cells. To this purpose, ppC were cultured as previously described (Brevini et al. 2007 Theriogenology 68, 206–214) and screened by RT-PCR for the two LIF receptor subunits (LRβ and gp130) and STAT3. Pig granulosa cells were used as positive controls. To better investigate the possible role of LIF in maintenance of pluripotency in ppC, the formation of embryoid bodies (EB) was induced in the presence or in the absence of the cytokine. Undifferentiated cells were cultured in hanging drops either with or without LIF for 12 days. The EB formation and the expression of molecular markers specific for the three germ layers was evaluated at the end of the differentiation period. Molecular analysis allowed us to detect transcription of STAT3, whereas no signal for LRβ and gp130 was detected in ppC. These results seem to indicate that LIF does not play a role in the maintenance of pluripotency in the pig. However, after removal of LIF, ppC routinely formed EB that expressed molecular markers specific for the three germ layers. On the other hand, when LIF was added to the differentiation medium, pig cells were unable to form EB. They kept proliferating in an undifferentiated state, and no expression of molecular markers specific for the three germ layers was detected. Moreover, when re-plated on inactivated feeder-layers, they formed distinct colonies that maintained expression of pluripotency markers. Our results show that a role of LIF in pluripotency maintenance through a classical LRβ-gp130 and STAT3 activation pathway is unlikely. However, interaction with an alternative nonclassical activation signaling pathway cannot be ruled out. Indeed, the presence of the cytokine in the medium used for differentiation experiments actively inhibited EB formation, indicating a possible role in preventing differentiation in the porcine species. Further studies are needed to elucidate these aspects. Supported by: PRIN2005; PRIN2006; First 2006; First2007.

scholarly journals PATH-65. MOLECULAR SIGNATURE OF FAT1 RELATED MOLECULES IN GLIOMAS IN THE CONTEXT OF THE WHO 2016 CLASSIFICATION

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi158-vi158
Author(s):  
Kunzang Chosdol ◽  
Manvi Arora ◽  
Nargis Malik ◽  
Prerana Jha ◽  
Jyotsna Singh ◽  
...  
Keyword(s):  
Molecular Markers ◽  
In Silico Analysis ◽  
Molecular Signature ◽  
World Health ◽  
Low Grade ◽  
Who Grade ◽  
Inflammatory Microenvironment ◽  
Molecular Features

Abstract Glioblastoma (GBM, WHO grade-IV) being the most malignant and aggressive form of glioma remains a major clinical challenge, with an overall 5-year survival rate of only 9.8%. Till recently, glioma diagnosis and grading were solely dependent on the phenotypic and histological features. However, with the advancement in the understanding of the molecular biology of glioma several molecules have been identified. The importance of these molecular/genotypic features of the tumor became evident by the inclusion of these molecular features by World Health Organization (WHO) in 2016 in glioma sub-grouping. Our lab is focused on studying the role of FAT1 gene (human ortholog of Drosophila tumor suppressor gene, fat) in glioma biology and aggressiveness. We observed FAT1 gene to have an oncogenic role in glioma where it has been found to upregulate migration/invasion, inflammatory microenvironment of the tumors, HIF1α expression/activity in the tumor-cells under severe hypoxia and in regulating EMT/stemness properties of GBM-cells under hypoxia. Here, we have characterized the molecular relationship between FAT1 related molecules and known- molecular markers of glioma with the hope of identifying glioma subgroup with a molecular signature of clinical significance by (i) analyzing the expression correlation of FAT1 and FAT1 regulated pro-inflammatroy molecules like COX2, IL1b and IL6 with the known- molecular markers of glioma like p53, IDH1, MGMT, EGFR, TERT in low-grade (grade-II) and high-grade (grade-III/IV) gliomas (n=50) by real-time PCR, sequencing, immunohistochemistry and in-silico analysis of TCGA-GBM-data (ii) Analyzed the regulatory role of FAT1 on the above known markers by siRNA mediated knockdown of FAT1 in in-vitro cell-culture system and (iii) further analyzed the identified molecular signature for their correlation with the patients prognosis/survival in the follow up patients. We observed a novel molecular signature with significant correlation with patients’ clinical outcome. Therapeutic targetting of FAT1 may benefit patients with high FAT1 expressing tumors.

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