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All Journal Biota Jurnal Ilmiah Wahana Pendidikan
Saarah Hamidah Asmara Indratno
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Religion Agriculture, Biological Sciences & Forestry Biochemistry, Genetics & Molecular Biology Education Environmental Science Materials Science & Nanotechnology Medicine & Pharmacology Social Sciences Other

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Review Artikel: Target Aksi Obat Antiepilepsi Terhadap Reseptor Kanal Ion Natrium Munir Alinu Mukti; Jekmal Malau; Saarah Hamidah Asmara Indratno; Shafira Intan Anggraini; Shinta Puspa Dwiyanti; Siti Nafisa; Siti Rohmah; Sofianti Hidayat
Jurnal Ilmiah Wahana Pendidikan Vol 9 No 2 (2023): Jurnal Ilmiah Wahana Pendidikan
Publisher : Peneliti.net

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (132.916 KB) | DOI: 10.5281/zenodo.7672710

Abstract

Ion channels are selective pore complexing proteins. One of the ions that can be passed is sodium ion (Na+). Disturbances in the sodium channel (Na+) can be caused epilepsy disease. Epilepsy is a neurological condition characterized by recurrent seizures caused by brief disorders of electrical function in the brain. The purpose of this review is to determine the sodium ion channel receptor as a target for the action of antiepileptic drugs. The method used is based on a literature study. A total of 17 journals through the Google Scholar search engine, PubMed, ScienceDirect, and Microbiology Textbook were applied. The result of analysis using the entire reference showed that the mechanism of action of anti-epileptic drugs is specific for inhibition of the Na+ which is known that depend on the action potential. Examples of drugs are Phenytoin, Carbamazepine, & Lamotrigine. Phenytoin works by binding and blocking active sodium ion channels to reduce the number of open channels along the axon/cell body so that it will inhibit high-frequency release by slowing channel replacement and blocking continuous sodium currents. In addition, Carbamazepine works by blocking Na+ channels, so that there is no influx/entry of Na+ into the nerve cells. It will be effect that excessive depolarization does not occur and seizures can be stopped immediately. Another drug, Lamotrigine is similar to Phenytoin and Carbamazepine. The mechanism is voltage-dependent sodium channel conductance, stabilizing the nerve membrane thereby modulating the release of presynaptic excitatory neurotransmitters and inhibiting presynaptic glutamate.
Comparison of Two PCR Primer Sets for In-House Validation of GHSR Gene Variation Detection Employing Artificial Recombinant Plasmid Approach Ahsanal Kasasiah; Jekmal Malau; Sekar Andjung Tresnawati; Priscinya Christiana Debora; Nur Komala Fitri; Saarah Hamidah Asmara Indratno; Asman Hitopik; Eriyanti Astika; Anisa Aula Rahma; Fikri, Al Mukhlas
Biota Vol 10 No 2 (2024): Jurnal Biota 2024
Publisher : Faculty of Science and Technology Universitas Islam Negeri Raden Fatah Palembang

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19109/biota.v10i2.21166

Abstract

Stunting is a significant global public health problem caused by long-term dietary deficits that affect many children worldwide. Both environmental and genetic factors, including variants in the GHSR gene, play a crucial role in stunted growth. This study used an artificial recombinant plasmid DNA method to evaluate two primer set combinations for identifying DNA variants in the GHSR gene. Selecting suitable primer sets for identifying GHSR genetic variants linked to stunting is essential, as evidenced by PCR and sequencing techniques. The target gene, based on the GHSR reference sequence, consists of eight DNA variations (ΔQ36, G57G, P108L, L118L, R159R, C173R, D246A, and A277P). A recombinant plasmid was created by inserting a 1000 bp fragment of the GHSR gene into the pUC57 backbone. Primer sets were chosen based on their capacity to amplify these eight genetic variations and were optimized and validated using PCR methods. PCR and bi-directional sequencing verified the existence of surrounding DNA and specific single nucleotide variants (SNVs). In our study, we discovered four changes in the DNA sequence (R159R G>A, C173R T>C, D246A A>C, and A277P G>C) using the E1_F2/E1_R3 primer pair. Additionally, a new combination of primers (E1_F1/E1_R3) effectively detected seven DNA sequence mutations (ΔQ36 del CAG, G57G C>T, P108L C>T, L118L C>T, R159R G>A, C173R T>C, and D246A A>C). We have developed a new combination of forward and reverse primers to identify seven SNVs in the GHSR gene, which could serve as a diagnostic tool in clinical laboratory settings.
Co-Authors Ahsanal Kasasiah Anisa Aula Rahma Asman Hitopik Eriyanti Astika Fikri, Al Mukhlas Jekmal Malau Munir Alinu Mulki Nur Komala Fitri Priscinya Christiana Debora Sekar Andjung Tresnawati Shafira Intan Anggraini Shinta Puspa Dwiyanti Siti Nafisa Siti Rohmah Sofianti Hidayat