Displaying publications 21 - 40 of 990 in total

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  1. Bukhari N, Leow ATC, Abd Rahman RNZR, Mohd Shariff F
    Molecules, 2020 Jul 28;25(15).
    PMID: 32731608 DOI: 10.3390/molecules25153433
    Rational design is widely employed in protein engineering to tailor wild-type enzymes for industrial applications. The typical target region for mutation is a functional region like the catalytic site to improve stability and activity. However, few have explored the role of other regions which, in principle, have no evident functionality such as the N-terminal region. In this study, stability prediction software was used to identify the critical point in the non-functional N-terminal region of L2 lipase and the effects of the substitution towards temperature stability and activity were determined. The results showed 3 mutant lipases: A8V, A8P and A8E with 29% better thermostability, 4 h increase in half-life and 6.6 °C higher thermal denaturation point, respectively. A8V showed 1.6-fold enhancement in activity compared to wild-type. To conclude, the improvement in temperature stability upon substitution showed that the N-terminal region plays a role in temperature stability and activity of L2 lipase.
    Matched MeSH terms: Mutation, Missense*
  2. Tang MM, Surana U, Leong KF, Pramano ZAD
    Int J Dermatol, 2021 Jul;60(7):e288-e290.
    PMID: 33728648 DOI: 10.1111/ijd.15523
    Matched MeSH terms: Mutation; Mutation, Missense
  3. Mat Ripen A, Ghani H, Chear CT, Chiow MY, Syed Yahya SNH, Kassim A, et al.
    SAGE Open Med, 2020;8:2050312120922652.
    PMID: 32547748 DOI: 10.1177/2050312120922652
    Objectives: A pair of female Malay monozygotic twins who presented with recurrent upper respiratory tract infections, hepatosplenomegaly, bronchiectasis and bicytopenia were recruited in this study. Both patients were suspected with primary immunodeficiency diseases. However, the definite diagnosis was not clear due to complex disease phenotypes. The objective of this study was to identify the causative gene mutation in these patients.

    Methods: Lymphocyte subset enumeration test and whole exome sequencing were performed.

    Results: We identified a compound heterozygous CR2 mutation (c.1916G>A and c.2012G>A) in both patients. These variants were then confirmed using Sanger sequencing.

    Conclusion: Whole exome sequencing analysis of the monozygotic twins revealed compound heterozygous missense mutations in CR2.

    Matched MeSH terms: Mutation; Mutation, Missense
  4. Soon BH, Abu N, Abdul Murad NA, Then SM, Abu Bakar A, Fadzil F, et al.
    Per Med, 2022 01;19(1):25-39.
    PMID: 34873928 DOI: 10.2217/pme-2021-0033
    Aim: Mitochondrial DNA (mtDNA) alterations play an important role in the multistep processes of cancer development. Gliomas are among the most diagnosed brain cancer. The relationship between mtDNA alterations and different grades of gliomas are still elusive. This study aimed to elucidate the profile of somatic mtDNA mutations in different grades of gliomas and correlate it with clinical phenotype. Materials & methods: Forty histopathologically confirmed glioma tissue samples and their matched blood were collected and subjected for mtDNA sequencing. Results & conclusion: About 75% of the gliomas harbored at least one somatic mutation in the mtDNA gene, and 45% of these mutations were pathogenic. Mutations were scattered across the mtDNA genome, and the commonest nonsynonymous mutations were located at complex I and IV of the mitochondrial respiratory chain. These findings may have implication for future research to determine the mitochondrial energetics and its downstream metabolomics on gliomas.
    Matched MeSH terms: Mutation/genetics
  5. Zainulabid UA, Mat Yassim AS, Hussain M, Aslam A, Soffian SN, Mohd Ibrahim MS, et al.
    PLoS One, 2022;17(2):e0263678.
    PMID: 35213571 DOI: 10.1371/journal.pone.0263678
    SARS-CoV-2 has spread throughout the world since its discovery in China, and Malaysia is no exception. WGS has been a crucial approach in studying the evolution and genetic diversity of SARS-CoV-2 in the ongoing pandemic. Despite considerable number of SARS-CoV-2 genome sequences have been submitted to GISAID and NCBI databases, there is still scarcity of data from Malaysia. This study aims to report new Malaysian lineages of the virus, responsible for the sustained spikes in COVID-19 cases during the third wave of the pandemic. Patients with nasopharyngeal and/or oropharyngeal swabs confirmed COVID-19 positive by real-time RT-PCR with CT value < 25 were chosen for WGS. The selected SARS-CoV-2 isolates were then sequenced, characterized and analyzed along with 986 sequences of the dominant lineages of D614G variants currently circulating throughout Malaysia. The prevalence of clade GH and G formed strong ground for the presence of two Malaysian lineages of AU.2 and B.1.524 that has caused sustained spikes of cases in the country. Statistical analysis on the association of gender and age group with Malaysian lineages revealed a significant association (p <0.05). Phylogenetic analysis revealed dispersion of 41 lineages, of these, 22 lineages are still active. Mutational analysis showed presence of unique G1223C missense mutation in transmembrane domain of the spike protein. For better understanding of the SARS-CoV-2 evolution in Malaysia especially with reference to the reported lineages, large scale studies based on WGS are warranted.
    Matched MeSH terms: Mutation*
  6. Liang JS, Hung KL, Lin LJ, Ong WP, Keng WT, Lu JF
    Epilepsy Behav, 2023 Aug;145:109266.
    PMID: 37385119 DOI: 10.1016/j.yebeh.2023.109266
    Zellweger spectrum disorders (ZSD) are rare autosomal recessive disorders caused by defects in peroxisome biogenesis factor (PEX; peroxin) genes leading to impaired transport of peroxisomal proteins with peroxisomal targeting signals (PTS). Four patients, including a pair of homozygotic twins, diagnosed as ZSD by genetic study with different clinical presentations and outcomes as well as various novel mutations are described here. A total of 3 novel mutations, including a nonsense, a frameshift, and a splicing mutation, in PEX1 from ZSD patients were identified and unequivocally confirmed that the p.Ile989Thr mutant PEX1 exhibited temperature-sensitive characteristics and is associated with milder ZSD. The nature of the p.Ile989Thr mutant exhibited different characteristics from that of the other previously identified temperature-sensitive p.Gly843Asp PEX1 mutant. Transcriptome profiles under nonpermissive vs. permissive conditions were explored to facilitate the understanding of p.Ile989Thr mutant PEX1. Further investigation of molecular mechanisms may help to clarify potential genetic causes that could modify the clinical presentation of ZSD.
    Matched MeSH terms: Mutation/genetics
  7. Kalle Kwaifa I, Lai MI, Md Noor S
    Orphanet J Rare Dis, 2020 06 29;15(1):166.
    PMID: 32600445 DOI: 10.1186/s13023-020-01429-1
    BACKGROUND: Defective synthesis of the α-globin chain due to mutations in the alpha-globin genes and/or its regulatory elements leads to alpha thalassaemia syndrome. Complete deletion of the 4 alpha-globin genes results in the most severe phenotype known as haemoglobin Bart's, which leads to intrauterine death. The presence of one functional alpha gene is associated with haemoglobin H disease, characterised by non-transfusion-dependent thalassaemia phenotype, while silent and carrier traits are mostly asymptomatic.

    MAIN BODY: Clinical manifestations of non-deletional in alpha thalassaemia are varied and have more severe phenotype compared to deletional forms of alpha thalassaemia. Literature for the molecular mechanisms of common non-deletional alpha thalassaemia including therapeutic measures that are necessarily needed for the understanding of these disorders is still in demand. This manuscript would contribute to the better knowledge of how defective production of the α-globin chains due to mutations on the alpha-globin genes and/or the regulatory elements leads to alpha thalassaemia syndrome.

    CONCLUSION: Since many molecular markers are associated with the globin gene expression and switching over during the developmental stages, there is a need for increased awareness, new-born and prenatal screening program, especially for countries with high migration impact, and for improving the monitoring of patients with α-thalassaemia.

    Matched MeSH terms: Mutation/genetics
  8. Lee JY, Bhandare RR, Boddu SHS, Shaik AB, Saktivel LP, Gupta G, et al.
    Biomed Pharmacother, 2024 Apr;173:116275.
    PMID: 38394846 DOI: 10.1016/j.biopha.2024.116275
    Tumour suppressor genes play a cardinal role in the development of a large array of human cancers, including lung cancer, which is one of the most frequently diagnosed cancers worldwide. Therefore, extensive studies have been committed to deciphering the underlying mechanisms of alterations of tumour suppressor genes in governing tumourigenesis, as well as resistance to cancer therapies. In spite of the encouraging clinical outcomes demonstrated by lung cancer patients on initial treatment, the subsequent unresponsiveness to first-line treatments manifested by virtually all the patients is inherently a contentious issue. In light of the aforementioned concerns, this review compiles the current knowledge on the molecular mechanisms of some of the tumour suppressor genes implicated in lung cancer that are either frequently mutated and/or are located on the chromosomal arms having high LOH rates (1p, 3p, 9p, 10q, 13q, and 17p). Our study identifies specific genomic loci prone to LOH, revealing a recurrent pattern in lung cancer cases. These loci, including 3p14.2 (FHIT), 9p21.3 (p16INK4a), 10q23 (PTEN), 17p13 (TP53), exhibit a higher susceptibility to LOH due to environmental factors such as exposure to DNA-damaging agents (carcinogens in cigarette smoke) and genetic factors such as chromosomal instability, genetic mutations, DNA replication errors, and genetic predisposition. Furthermore, this review summarizes the current treatment landscape and advancements for lung cancers, including the challenges and endeavours to overcome it. This review envisages inspired researchers to embark on a journey of discovery to add to the list of what was known in hopes of prompting the development of effective therapeutic strategies for lung cancer.
    Matched MeSH terms: Mutation/genetics
  9. Ishak SNH, Kamarudin NHA, Ali MSM, Leow ATC, Rahman RNZRA
    Molecules, 2020 Jul 28;25(15).
    PMID: 32731607 DOI: 10.3390/molecules25153430
    A comparative structure analysis between space- and an Earth-grown T1 recombinant lipase from Geobacillus zalihae had shown changes in the formation of hydrogen bonds and ion-pair interactions. Using the space-grown T1 lipase validated structure having incorporated said interactions, the recombinant T1 lipase was re-engineered to determine the changes brought by these interactions to the structure and stability of lipase. To understand the effects of mutation on T1 recombinant lipase, five mutants were developed from the structure of space-grown T1 lipase and biochemically characterized. The results demonstrate an increase in melting temperature up to 77.4 °C and 76.0 °C in E226D and D43E, respectively. Moreover, the mutated lipases D43E and E226D had additional hydrogen bonds and ion-pair interactions in their structures due to the improvement of stability, as observed in a longer half-life and an increased melting temperature. The biophysical study revealed differences in β-Sheet percentage between less stable (T118N) and other mutants. As a conclusion, the comparative analysis of the tertiary structure and specific residues associated with ion-pair interactions and hydrogen bonds could be significant in revealing the thermostability of an enzyme with industrial importance.
    Matched MeSH terms: Mutation, Missense*
  10. Ibrahim RW, Ahmad MZ, Al-Janaby HF
    Saudi J Biol Sci, 2016 Jan;23(1):S45-9.
    PMID: 26858564 DOI: 10.1016/j.sjbs.2015.09.012
    A mutation is ultimately essential for adaptive evolution in all populations. It arises all the time, but is mostly fixed by enzymes. Further, most do consider that the evolution mechanism is by a natural assortment of variations in organisms in line for random variations in their DNA, and the suggestions for this are overwhelming. The altering of the construction of a gene, causing a different form that may be communicated to succeeding generations, produced by the modification of single base units in DNA, or the deletion, insertion, or rearrangement of larger units of chromosomes or genes. This altering is called a mutation. In this paper, a mathematical model is introduced to this reality. The model describes the time and space for the evolution. The tool is based on a complex domain for the space. We show that the evolution is distributed with the hypergeometric function. The Boundedness of the evolution is imposed by utilizing the Koebe function.
    Matched MeSH terms: Mutation
  11. George E
    PMID: 8629111
    Beta-thalassemia in West Malaysia is caused by 14 molecular defects with differing clinical severity. In Chinese patients from West Malaysia, the main beta-thalassemia mutations seen were (a) a 4 base pair-TCTT deletion in codon 41-42 [frameshift mutation (FSC 41-42)]; (b) a C to T substitution at the second intervening sequence (IVS2-654); (c) an A to G substitution in the TATA box [-28 (A to G)], and (d) an A to T substitution in codon 17[17 A to T]. In the Malays, the main mutations seen were (a) a G to C in nucleotide 5 at the intervening sequence I [IVS1-5 (G to C)]; (b) G to T substitution in nucleotide I at the intervening sequence I [IVS1-1 (G to T)]; (c) a A to T substitution in codon 17 (17 A to T); (d) removal of C from codon 35 [codon 35 (-C)], and (e) a 4 base pairs-TCTT deletion in codon 41-42 [frameshift mutation (FSC 41-42)]. A scoring system (Tha1 CS) has been formulated to predict clinical severity. It is the type of beta-thalassemia mutation present that decides on the clinical phenotype. The most severe beta-thalassemia mutation is assigned a score of 4. A score of 8 indicates severe thalassemia.
    Matched MeSH terms: Frameshift Mutation*; Point Mutation*
  12. How VJ
    Malays J Pathol, 1990 Jun;12(1):59-60.
    PMID: 2090890
    Matched MeSH terms: Mutation
  13. Kwong A, Shin VY, Ho JC, Kang E, Nakamura S, Teo SH, et al.
    J Med Genet, 2016 Jan;53(1):15-23.
    PMID: 26187060 DOI: 10.1136/jmedgenet-2015-103132
    Approximately 5%-10% of breast cancers are due to genetic predisposition caused by germline mutations; the most commonly tested genes are BRCA1 and BRCA2 mutations. Some mutations are unique to one family and others are recurrent; the spectrum of BRCA1/BRCA2 mutations varies depending on the geographical origins, populations or ethnic groups. In this review, we compiled data from 11 participating Asian countries (Bangladesh, Mainland China, Hong Kong SAR, Indonesia, Japan, Korea, Malaysia, Philippines, Singapore, Thailand and Vietnam), and from ethnic Asians residing in Canada and the USA. We have additionally conducted a literature review to include other Asian countries mainly in Central and Western Asia. We present the current pathogenic mutation spectrum of BRCA1/BRCA2 genes in patients with breast cancer in various Asian populations. Understanding BRCA1/BRCA2 mutations in Asians will help provide better risk assessment and clinical management of breast cancer.
    Matched MeSH terms: Mutation*; Germ-Line Mutation*
  14. Chong YM, Sam IC, Ponnampalavanar S, Syed Omar SF, Kamarulzaman A, Munusamy V, et al.
    Microbiol Resour Announc, 2020 May 14;9(20).
    PMID: 32409547 DOI: 10.1128/MRA.00383-20
    We sequenced four severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genomes from Malaysia during the second wave of infection and found unique mutations which suggest local evolution. Circulating Malaysian strains represent introductions from different countries, particularly during the first wave of infection. Genome sequencing is important for understanding local epidemiology.
    Matched MeSH terms: Mutation
  15. Mahajan A, Buse J, Kline G
    Osteoporos Int, 2020 Jan;31(1):203-207.
    PMID: 31641801 DOI: 10.1007/s00198-019-05170-9
    Familial hypocalciuric hypercalcemia (FHH) is a benign autosomal dominant condition characterized by lifelong asymptomatic hypercalcemia. FHH is typically caused by a heterozygous inactivating mutation of the calcium-sensing receptor (CaSR) and characterized by moderate hypercalcemia, inappropriately normal or elevated serum parathyroid hormone (PTH), and relative hypocalciuria (FeCa  2%. PTH levels were repeatedly below the mean of the reference range (on two separate assays) and sometimes even below the lower reference limit. Two siblings, one niece, and her son had hypercalcemia without nephrolithiasis. Cinacalcet, used as a PTH-suppression test, normalized serum total and ionized calcium after 7 days of cinacalcet 30 mg BID, confirming her hypercalcemia was PTH-mediated. Given her family history, genetic testing was pursued and discovered a novel pathogenic mutation of the CaSR gene confirming the diagnosis of FHH type 1. Our case represents an atypical presentation of FHH1 with low PTH and FeCa > 2%. This contributes to the expanding clinical and biochemical spectrum of CaSR inactivating mutations and presents an innovative approach to evaluating biochemically uncertain familial hypercalcemia with cinacalcet before pursuing expensive genetic analysis.
    Matched MeSH terms: Mutation
  16. Dulyayangkul P, Wan Nur Ismah WAK, Douglas EJA, Avison MB
    Antimicrob Agents Chemother, 2020 06 23;64(7).
    PMID: 32312773 DOI: 10.1128/AAC.02208-19
    Meropenem-vaborbactam resistance in Klebsiella pneumoniae isolates is associated with loss-of-function mutations in the OmpK35 and OmpK36 porins. We identify two previously unknown loss-of-function mutations that confer cefuroxime resistance in K. pneumoniae isolates. The proteins lost were NlpD and KvrA; the latter is a transcriptional repressor that controls capsule production. We demonstrate that KvrA loss reduces OmpK35 and OmpK36 porin production, which confers reduced susceptibility to meropenem-vaborbactam in a KPC-3-producing K. pneumoniae isolate.
    Matched MeSH terms: Mutation
  17. Wang S, Liu Q, Liu Y, Jia H, Abualigah L, Zheng R, et al.
    Comput Intell Neurosci, 2021;2021:6379469.
    PMID: 34531910 DOI: 10.1155/2021/6379469
    Based on Salp Swarm Algorithm (SSA) and Slime Mould Algorithm (SMA), a novel hybrid optimization algorithm, named Hybrid Slime Mould Salp Swarm Algorithm (HSMSSA), is proposed to solve constrained engineering problems. SSA can obtain good results in solving some optimization problems. However, it is easy to suffer from local minima and lower density of population. SMA specializes in global exploration and good robustness, but its convergence rate is too slow to find satisfactory solutions efficiently. Thus, in this paper, considering the characteristics and advantages of both the above optimization algorithms, SMA is integrated into the leader position updating equations of SSA, which can share helpful information so that the proposed algorithm can utilize these two algorithms' advantages to enhance global optimization performance. Furthermore, Levy flight is utilized to enhance the exploration ability. It is worth noting that a novel strategy called mutation opposition-based learning is proposed to enhance the performance of the hybrid optimization algorithm on premature convergence avoidance, balance between exploration and exploitation phases, and finding satisfactory global optimum. To evaluate the efficiency of the proposed algorithm, HSMSSA is applied to 23 different benchmark functions of the unimodal and multimodal types. Additionally, five classical constrained engineering problems are utilized to evaluate the proposed technique's practicable abilities. The simulation results show that the HSMSSA method is more competitive and presents more engineering effectiveness for real-world constrained problems than SMA, SSA, and other comparative algorithms. In the end, we also provide some potential areas for future studies such as feature selection and multilevel threshold image segmentation.
    Matched MeSH terms: Mutation
  18. Soh LS, Veera Singham G
    Pest Manag Sci, 2021 Nov;77(11):5202-5212.
    PMID: 34272799 DOI: 10.1002/ps.6561
    BACKGROUND: The common bed bug, Cimex lectularius L., and the tropical bed bug, Cimex hemipterus (F.), are now widely regarded as important public health pests following their rapid global resurgence, largely due to insecticide resistance and an increased rate of global travel. The insecticide resistance mechanisms are well documented in C. lectularius, however, only one mechanism is validated in C. hemipterus thus far. This demands further understanding on the resistance mechanisms involved in C. hemipterus.

    RESULTS: Here, we identified differences in resistance to fenitrothion (organophosphate) and imidacloprid (neonicotinoid) related cuticle thickness in C. hemipterus. There is evidence of a possible association between cuticle thickness and resistance, but the association can be tenuous, likely because resistance is multifactorial in C. hemipterus. We also discovered a novel T1011 residue in domain IIS6 of the voltage-gated sodium channel that likely enhanced susceptibility to deltamethrin (pyrethroid) despite the presence of a L1014F mutation known to confer pyrethroid resistance in C. hemipterus. Our findings also confirmed that the M918I mutation enhanced resistance to pyrethroid when present with the L1014F mutation, which was consistent with a super-kdr phenotype, as reported previously. Multiple resistance mechanisms can be found within a single C. hemipterus population, and the presence of both M918I + L1014F mutations likely masked the influence of cuticle thickness in conferring resistance against deltamethrin. The elevated metabolic enzyme activities in some strains were not necessarily associated with increased insecticide resistance.

    CONCLUSION: This study has enhanced our understanding on the penetration resistance mechanism and target site insensitivity of sodium channels in C. hemipterus.

    Matched MeSH terms: Mutation
  19. Sa'at H, Lee YK, Yoon SY, Wong SW, Woo YL, Barlow-Stewart K, et al.
    Int J Behav Med, 2022 Feb;29(1):1-13.
    PMID: 33791992 DOI: 10.1007/s12529-021-09984-y
    BACKGROUND: The uptake of risk-reducing salpingo-oophorectomy (RRSO) in Asian countries is variable despite being the most effective option for ovarian cancer risk reduction in BRCA mutation carriers. Exploration of factors which may impact the RRSO decision-making of BRCA mutation carriers from Malaysia, a developing country in Southeast Asia, was undertaken.

    METHODS: In-depth interviews with 28 Malaysian BRCA mutation carriers with a history of breast cancer were conducted in addition to observing their RRSO decision-making consultations in the clinic.

    RESULTS: The decision-making considerations among the carriers were centered around the overarching theme of "Negotiating cancer risk and womanhood priorities," with the following themes: (1) risk perception, (2) self-preservation, (3) motherhood obligation, and (4) the preciousness of marriage. Cognitive knowledge of BRCA risk was often conceptualized based on personal and family history of cancer, personal beliefs, and faith. Many women reported fears that RRSO would affect them physically and emotionally, worrying about the post-surgical impact on their motherhood responsibilities. Nevertheless, some reported feeling obliged to choose RRSO for the sake of their children. For some, their husband's support and approval were critical, with emotional well-being and sexuality reportedly perceived as important to sustaining married life. Despite reporting hesitancy toward RRSO, women's decisions about choosing this option evolved as their priorities changed at different stages of life.

    CONCLUSIONS: Recognizing during clinic encounters with Malaysian women that RRSO decision-making involves negotiating the likelihood of developing cancer with the societal priorities of being a woman, mother, and wife may serve to support their decision-making.

    Matched MeSH terms: Mutation
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