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MUTYH protein, human

MUTYH is a DNA glycosylase enzyme that plays a crucial role in base excision repair, specifically in the removal of 8-oxoguanine from DNA.
This protein helps maintain genomic integrity by preventing the accumulation of G:C to T:A transversions, which can lead to oncogenic mutations.
MUTYH-associated polyposis (MAP) is an autosomal recessive disorder characterized by the development of multiple colorectal adenomas and an increased risk of colorectal cancer.
Researchers studying MUYTM protein can leverae PubCompare.ai, an AI-driven platform, to optimize protocols, enhance reproducibility, and locate the best research protocols from literature, preprints, and patents.

Most cited protocols related to «MUTYH protein, human»

1
Genetic Screening for Familial Hypercholesterolemia and Colorectal Cancer

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Publication 2018
APOB protein, human BMPR1A protein, human Cardiovascular Diseases Colonic Polyps Genes Genetic Diversity Genome, Human Hypercholesterolemia LDLR protein, human MLH1 protein, human MSH6 protein, human MUTYH protein, human Nucleotides Patient Acceptance of Health Care PCSK9 protein, human Pharmaceutical Preparations PMS2 protein, human Point-of-Care Systems POLD1 protein, human Reproduction SMAD4 protein, human
2
Genetic modeling of colorectal cancer risk
We used modified segregation analysis to fit a range of genetic models to the
observed colorectal cancer family histories for the proband and their first-degree
relatives. Individuals were assumed to be at risk of colorectal cancer from birth until
the earliest of the following: diagnosis of colorectal cancer or any other cancer (except
skin cancer); first polypectomy; death; and the earlier of last known age at baseline
interview or age 80 years.
The colorectal cancer incidence
λi(t,k) for
individual i at age t in sex group k(k = 1 for males or 2 for females) was assumed to depend on
genotype according to a parametric survival analysis model
λi(t,k)=λ0(t,k)
exp(Gi+Pi(t)), where
λ0(t,k) is the
sex-specific baseline incidence at age t. Giis the natural logarithm of the relative risk associated with the major genotype and
Pi(t) is the polygenic component for age
t.
The major genotype was defined by six components representing each of the genes
MLH1, MSH2, MSH6, PMS2, MUTYH and one representing the hypothetical
unidentified major genes. We fitted models in which the unidentified major genes were
autosomal with a normal and a mutant allele unlinked to mutations in the MMR genes or
MUTYH. We also fitted models in which the average relative risk for the
unidentified major genes was assumed to be age dependent. We used the published age-, sex-
and country-specific incidences for MLH1 and MSH2mutation carriers (32 (link)), and published age- and
sex-specific incidences for MSH6, PMS2 and MUTYHmutation carriers (26 (link), 33 (link), 34 (link)).
The polygenic component for age t,
Pi(t), was assumed to be normally
distributed with zero mean and variance
σ2p(t).
P was approximated by the hypergeometric polygenic model (35 (link), 36 ). We also
fitted models where the variance of the polygenic ‘modifying’ component
was allowed to take a different value σ2mfor MMR gene and MUTYH carriers.
To compute the baseline colorectal cancer incidence
λ0(t), we constrained the overall
incidence of colorectal cancer to agree with the national age- and sex-specific incidences
(1998–2002) separately for Australia, Canada and USA (37 ). Other cancers were ignored in this model.
We assumed that the sensitivity of the mutation testing of probands for MMR
genes and MUTYH was 80%,(38 (link)) and we examined the effect of varying this sensitivity. For relatives, we
assumed the mutation screening for the proband’s mutation (i.e. predictive
testing) was 100% sensitive and specific.
The genetic models were specified in terms of colorectal cancer incidence for
MMR gene and MUTYH mutation carriers, the frequency
(qA) of the putative high risk allele “A” of
the unidentified major genes component, the average relative risk of colorectal cancer for
carriers of mutations in the unidentified major genes, and the variances of the polygenic
and modifying components (σ2p and
σ2m). Maximum likelihood estimation was
used to estimate parameters. The estimates we present are the values that were the most
likely (i.e. most consistent) with the data. Maximum likelihood is the optimal method for
making such estimates, and provides confidence intervals (CIs). We adjusted for
ascertainment by maximizing the likelihood of each pedigree conditioned on the colorectal
cancer status of the proband and his or her age of diagnosis (but not the mutation carrier
status as this information was not known at the time of recruitment).
The relative goodness of fit for nested models was tested by the likelihood
ratio test. The Akaike’s Information Criterion(39 ) [AIC=−2×log-likelihood +
2×(no. of parameters)] was used to assess goodness of fit between non-
nested models (40 ).
The expected versus observed number of affected relatives under each fitted
model was assessed using the Pearson χ2 goodness of fit statistic. The
expected number of probands with MMR and MUTYH mutation carriers for
families that had undergone mutation testing based on their cancer family history was
computed using Bayes theorem (41 (link)). Statistical
methods are described further in the Appendix.
Win A.K., Jenkins M.A., Dowty J.G., Antoniou A.C., Lee A., Giles G.G., Buchanan D.D., Clendenning M., Rosty C., Ahnen D.J., Thibodeau S.N., Casey G., Gallinger S., Le Marchand L., Haile R.W., Potter J.D., Zheng Y., Lindor N.M., Newcomb P.A., Hopper J.L, & MacInnis R.J. (2016). Prevalence and Penetrance of Major Genes and Polygenes for Colorectal Cancer. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 26(3), 404-412.
Publication 2016
Alleles Childbirth Colorectal Carcinoma Diagnosis Females Gene Components Genes Genotype Hypersensitivity Males Malignant Neoplasms MLH1 protein, human MSH6 protein, human Mutation MUTYH protein, human PMS2 protein, human
3
Targeted NGS Analysis of Cancer Genes
For targeted NGS analysis, Ion AmpliSeq designer software (Life Technologies, Tokyo, Japan) was used to design primers, which consisted of 610 primer pairs in two pools covering the exons and exon–intron boundaries of 25 cancer-predisposing genes (APC, ATM, BARD1, BMPR1A, BRIP1, CDH1, CDK4, CDKN2A, CHEK2, EPCAM, MLH1, MRE11A, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, PTEN, RAD50, RAD51C, RAD51D, SMAD4, STK11, and TP53) (Walsh et al. 2011 (link); Couch et al. 2014b (link); Economopoulou et al. 2015 (link); Tung et al. 2015 (link)). Multiplex polymerase chain reaction (PCR) was performed using 50–100 ng genomic DNA with 17 cycles with a premixed primer pool using Ion AmpliSeq Library Kit 2.0, as previously described (Hirotsu et al. 2014 (link)). The PCR amplicons were treated with 2 μL FuPa reagent to partially digest primer sequences and phosphorylate the amplicons. The amplicons were ligated to adapters with the diluted barcodes of the Ion Xpress Barcode Adapters kit (Life Technologies). Adaptor-ligated amplicon libraries were purified using Agencourt AMPure XP reagents (Beckman Coulter, Tokyo, Japan). The library concentration was determined using an Ion Library Quantitation Kit (Life Technologies), then each library was diluted to 8 pM and the same amount of libraries was pooled for one sequence reaction. Next, emulsion PCR was carried out using the Ion OneTouch System and Ion PI Template OT2 200 Kit v2 (Life Technologies) according to the manufacturer’s instructions. Template-positive Ion Sphere Particles were then enriched with Dynabeads MyOne Streptavidin C1 Beads (Life Technologies) using an Ion OneTouch ES system (Life Technologies). Purified Ion Sphere particles were loaded on an Ion PI Chip v2. Massively parallel sequencing was carried out on an Ion Proton System (Life Technologies) using the Ion PI Sequencing 200 Kit v2. Sequencing was performed using 500 flow runs that generated ∼200 bp reads.
Hirotsu Y., Nakagomi H., Sakamoto I., Amemiya K., Oyama T., Mochizuki H, & Omata M. (2015). Multigene panel analysis identified germline mutations of DNA repair genes in breast and ovarian cancer. Molecular Genetics & Genomic Medicine, 3(5), 459-466.
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Publication 2015
Aleurites alpha-fluoro-beta-ureidopropionic acid BMPR1A protein, human CDH1 protein, human CDKN2A Gene CHEK2 protein, human DNA Chips DNA Library Emulsions Exons Gene, Cancer Genome Introns MLH1 protein, human MRE11 protein, human MSH6 protein, human Multiplex Polymerase Chain Reaction MUTYH protein, human Oligonucleotide Primers Oncogenes PALB2 protein, human PI 200 PMS2 protein, human Polymerase Chain Reaction Protons PTEN protein, human Rad50 protein, human RAD51C protein, human SMAD4 protein, human STK11 protein, human Streptavidin TACSTD1 protein, human TP53 protein, human
4
Whole Exome Sequencing of Colorectal Cancer
CRC-affected individuals with tumour and matched germline whole exome sequencing (WES) data from five studies were included in the analysis: the Australasian (ACCFR) and Ontario (OCCFR) sites of the Colon Cancer Family Registry [22 (link),23 (link)], the ANGELS study, WEHI study and The Cancer Genome Atlas (TCGA) colon adenocarcinoma (COAD) and rectum adenocarcinoma (READ) study [24 (link)] (Figure 1, Supplementary Table 1, Supplementary Table 2). Formalin-fixed paraffin embedded (FFPE) CRCs from carriers of germline PVs in MLH1, MSH2 or MSH6 (n=33), from biallelic or monoallelic carriers of PVs in MUTYH (n=21) and from an individual carrying a PV and a VUS in MUTYH were included. Tumour MMR status was determined by immunohistochemistry with details of the tumour and germline characterisation undertaken described previously [25 (link),26 (link)]. Two groups of FFPE CRCs were selected as non-hereditary controls: 1) MMR-proficient (MMRp) CRCs without a known germline mutation in the MUTYH or MMR genes were included as “MMRp controls” (n=160), and 2) MMR-deficient (MMRd) CRCs resulting from somatic MLH1 gene promoter hypermethylation were included as “MMRd controls” (n=25). Tumours were then separated into discovery (n=142) and validation groups (n=97) based on their recruitment origin from either clinic-based (discovery) or population-based (validation). Furthermore, 498 CRC tumours from TCGA COAD and READ studies [24 (link)] were included as an additional set of fresh-frozen, non-hereditary CRCs (Supplementary Table 2). MMR status was determined using MSIseq [27 (link)], enabling stratification into 446 MMRp (“TCGA MMRp controls”) and 52 MMRd (“TCGA MMRd controls”), where each of the 52 MMRd controls were confirmed to have tumour hypermethylation of the MLH1 gene promoter (Supplementary Methods).
Georgeson P., Pope B.J., Rosty C., Clendenning M., Mahmood K., Joo J.E., Walker R., Hutchinson R., Preston S., Como J., Joseland S., Win A.K., Macrae F.A., Hopper J.L., Mouradov D., Gibbs P., Sieber O.M., O’Sullivan D.E., Brenner D.R., Gallinger S., Jenkins M.A., Winship I.M, & Buchanan D.D. (2021). Evaluating the utility of tumour mutational signatures for identifying hereditary colorectal cancer and polyposis syndrome carriers. Gut, 70(11), 2138-2149.
Publication 2021
Adenocarcinoma Calcibiotic Root Canal Sealer Cancer of Colon Colon Adenocarcinomas Colonic Neoplasms Diploid Cell Formalin Freezing Genes Genes, Neoplasm Genome Germ-Line Mutation Germ Line Immunohistochemistry Malignant Neoplasms MLH1 protein, human MSH6 protein, human MUTYH protein, human Neoplasms Paraffin Embedding Promoter, Genetic Rectum Reproduction
5
Inducible shRNA and MYH Overexpression Plasmid Generation
The shRNA plasmids were generated by cloning oligonucleotide from TRC library (Supplementary Table S1) into an inducible shRNA vector system, created through modifying pRSITEP-U6Tet-(sh)-EF1-TetRep-2A-Puro plasmid (Cellecta, Inc., Mountain View, CA, USA) by replacing the TetRep-2A-Puromycin site with either TetRep-P2A-Puro-P2A-RFP670 or TetRep-P2A-Puro-P2A-GFP. The vector contains a 1.2 kb stuffer sequence that was double–digested by FastDigest BshTI and EcoRI (FD1464 and FD0274; Thermo Fisher, Waltham, MA, USA) for 1 h. The 8 kb BshTI/EcoRI band was extracted from 1% agarose gel using Wizard SV Gel and PCR Clean-Up System (A9280; Promega, Madison, WI, USA). Separate forward and reverse oligos (custom DNA oligo service; Sigma) were annealed in the annealing buffer (10 mM Tris-HCl, pH 7.5, 0.1 M NaCl and 1 mM EDTA) using a thermal cycler (C1000; Bio-Rad), incubating for 5 min at 95 °C and then cooling gradually to 20 °C, and 1 μl of annealed oligo pairs was ligated into 50–100 ng of the digested vector using T4 DNA ligase (EL0014; Thermo Fisher) and T4 Polynucleotide Kinase (EK0031; Thermo Fisher), incubated overnight at 37 °C. Transformation was conducted using One Shot Stbl3 Chemically Competent Cells (C737303; Thermo Fisher) according to the manufacturer's protocol. Next, at least three colonies were picked for colony PCR using DreamTaq Green PCR Master Mix (K1081; Thermo Fisher). The primers used for this reaction were U6-tet-F: 5′-GGA CTA TCA TAT GCT TAC CGT AAC-3′ and U6-tet-R: 5′-TGG ATG AAT ACT GCC ATT TGT CTC-3′. Colonies lacking the stuffer were sent for sequencing (à la Carte Sequencing Service; Eurofins Genomics, Ebersberg, Germany). After sequencing validation of the constructs, a GFP reporter from pRSITEP-V2-GFP vector replaced the RFP670 cassette using double-digest reactions with FastDigest SalI and FastDigest XbaI (FD0644 and FD0684; Thermo Fisher).
The γ3-hMYH overexpression plasmid was generated by PCR amplification of MYH cDNA (GenBank accession number AF527839.1) using the following primers: 5′-TAT AGT CGA CAT GAG GAA GCC ACG-3′ and 5′-TAT AGC GGC CGC TCA CTG GGC TGC ACT G-3′. Double digestion reactions were carried out with FastDigest SalI and NotI (FD0644 and FD0593; Thermo Fisher) for 1 h. The PCR product was then ligated into pENTR1A no ccDB (17398; Addgene, Cambridge, MA, USA) entry vector using T4 DNA ligase (EL0014; Thermo Fisher). The entry vectors carrying γ3-hMYH insert were verified by sequencing (Eurofins Genomics). Next, the insert from entry vector was transferred to pINDUCER20 (44012; Addgene) destination vector using Gateway LR Clonase II (11791100; Thermo Fisher). Finally, the constructs were validated by colony PCR using DreamTaq Green PCR Master Mix (K1081; Thermo Fisher).
Eshtad S., Mavajian Z., Rudd S.G., Visnes T., Boström J., Altun M, & Helleday T. (2016). hMYH and hMTH1 cooperate for survival in mismatch repair defective T-cell acute lymphoblastic leukemia. Oncogenesis, 5(12), e275-.
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Publication 2016
2',5'-oligoadenylate 5'-chloroacetamido-5'-deoxythymidine Buffers Cells Cloning Vectors Deoxyribonuclease EcoRI Digestion DNA, Complementary DNA Library Edetic Acid MUTYH protein, human Oligonucleotide Primers Oligonucleotides Plasmids Polynucleotide 5'-Hydroxyl-Kinase Promega Puromycin Sepharose Short Hairpin RNA Sodium Chloride T4 DNA Ligase Tromethamine

Most recents protocols related to «MUTYH protein, human»

1
Hereditary Cancer Gene Variant Screening
Blood samples were collected in EDTA containing tubes. Genomic DNA was isolated with QIAamp DNA Mini QIAcube kit (QIAGEN, Germany) according to the manufacturer’s instructions. DNA concentrations were measured with the QubitTM Fluorometric Quantitation system (Thermo Fisher Scientific) using Qubit HS DNA Assay kit (Thermo Scientific, US). DNA libraries were obtained using the BRCA Hereditary Cancer MASTR Plus, Multiplicom (Agilent, United States) kit. Variant screening on 26 risk carrying genes for hereditary cancers like breast, ovarian and colorectal cancer (ABRAXAS1, ATM, BARD1, BLM, BRCA1, BRCA2, BRIP1, CDH1, CHEK2, EPCAM, MEN1, MLH1, MRE11, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, PTEN, RAD50, RAD51C, RAD51D, STK11, TP53, and XRCC2) has been performed by this kit which contained five multiplex PCR primer pools. 10 ng of DNA per primer pool was used for multiplex PCR amplification, followed by barcode ligation and purification with Agentcourt AMPureXP reagent (Beckman Coulter, Beverly, MA, United States). Quantity and quality of prepared libraries were assessed by QubitTM Fluorometric Quantitation system (Thermo Fisher Scientific). For library preparation 4 ng DNA was used. After libraries were prepared, sequence analysis was performed with Illumina MiSeq instrument using MiSeq Reagent v3 kit (Illumina, US). All sequencing data were submitted to Sequence Read Archive (SRA) (https://www.ncbi.nlm.nih.gov/sra/PRJNA895859).
Bioinformatics analysis was performed using the software Sophia Genetics DDM (Sophia Genetics v4.2). GRCh37/hg19 was used as the reference genome. During variant calling, a minimum sequence coverage depth and variant fraction parameters were set to 30x and 20%, respectively. Variants were classified according to the ACMG Guidelines (Richards et al., 2015 (link)) using databases of ClinVar (Landrum et al., 2014 (link)), BRCAExchange, OMIM®, dbSNP (v.155), gnomAD (v2.1.1), in silico pathogenicity classifiers of MutationTaster (Schwarz et al., 2010 (link)), SIFT (Ng and Henikoff, 2003 (link)), PolyPhen-2 (Adzhubei et al., 2013 ), REVEL (Ioannidis et al., 2016 (link)). All variants with minor allele frequency (MAF2) of less than 1% in gnomAD database were considered.
Keskin Karakoyun H., Yüksel Ş.K., Amanoglu I., Naserikhojasteh L., Yeşilyurt A., Yakıcıer C., Timuçin E, & Akyerli C.B. (2023). Evaluation of AlphaFold structure-based protein stability prediction on missense variations in cancer. Frontiers in Genetics, 14, 1052383.
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Publication 2023
Biological Assay BLOOD BRCA1 protein, human Breast Cancer, Familial CDH1 protein, human CHEK2 protein, human Colorectal Carcinoma DNA Library Edetic Acid Fluorometry Gene, BRCA2 Genetic Diversity Genome Ligation Malignant Neoplasms MLH1 protein, human MSH6 protein, human Multiple Endocrine Neoplasia Type 1 Multiplex Polymerase Chain Reaction MUTYH protein, human Oligonucleotide Primers Ovary PALB2 protein, human Pathogenicity PMS2 protein, human PTEN protein, human Rad50 protein, human RAD51C protein, human STK11 protein, human TACSTD1 protein, human TP53 protein, human XRCC2 protein, human
2
Rare Variant Analysis of Hereditary CRC
We used ANNOVAR [29 (link)] to annotate the VCF files from the 200,643 WES samples. The Genome Aggregation Database (gnomAD) [30 (link)] were used to retrieve variant frequencies from the general population. We focused on rare PV for hereditary CRC (Lynch syndrome, polyposis) and considered the same variant filtering approach that was used in a recent study aiming at selecting rare PV [31 (link)]. The following inclusion criteria were used: (1) only APC, MUTYH, MLH1, MSH2, MSH6, PMS2 variants in protein-coding regions were included since PV in other genes associated with hereditary CRC are too rare or even absent in the study population; (2) allele frequency (AF) < 0.005 in at least one ethnic subpopulation of gnomAD; (3) not annotated as “synonymous,” “non-frameshift deletion” and “non-frameshift insertion”; (4) annotated as “pathogenic” or “likely pathogenic” based on ClinVar [32 (link)]. We did not include MUTYH in the pooled analysis since no biallelic (i.e. high penetrance) case was identified in the cohort; however, we included the heterozygous (monoallelic) carriers in the single gene analysis to compare the effect size with the other genes.
Hassanin E., Spier I., Bobbili D.R., Aldisi R., Klinkhammer H., David F., Dueñas N., Hüneburg R., Perne C., Brunet J., Capella G., Nöthen M.M., Forstner A.J., Mayr A., Krawitz P., May P., Aretz S, & Maj C. (2023). Clinically relevant combined effect of polygenic background, rare pathogenic germline variants, and family history on colorectal cancer incidence. BMC Medical Genomics, 16, 42.
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Publication 2023
Deletion Mutation Ethnicity Frameshift Mutation Genes Genome Hereditary Nonpolyposis Colorectal Cancer Heterozygote MLH1 protein, human MSH6 protein, human Mutant Proteins MUTYH protein, human Pathogenicity PMS2 protein, human Strains
3
Genetic Polymorphism Analysis Protocol
The frequency of polymorphic variants of genes XRCC1 (rs25487), XRCC2 (rs3218536), OGG1 (rs1052133), UNG (rs246079 and rs151095402), RAD51 (rs1801320, rs7180135, rs1801321, and rs2619681), RAD51B (rs963917, rs963918, rs3784099, and rs10483813), SMUG1 (rs3087404), TP53 (rs1042522), RAD52 (rs1051669), MBD4 (rs2307293), MUTYH (rs3219472, rs3219489, and rs3219493), MRE11A (rs2155209), NBS1 (rs2735383), XRCC6 (rs132774), XRCC5 (rs207906), PRKDC (rs7003908), TDG (rs4135054), EXO1 (rs1776180), and XRCC3 (rs861539) was determined using TaqMan® SNP Genotyping Assays and the TaqMan Universal PCR Master Mix, No UNG (Applied Biosystems, Foster City, CA, USA). The total volume of PCR reaction was 20 μL, including 4 µL 5× HOT FIREPol® Probe qPCR Mix (Solis, Tartu, Estonia), 1 µL DNA (100 ng), 1 ul 20× TaqMan SNP primers, and 14 µL RNA free water. PCR reaction conditions were as follows: polymerase activation (10 min, 95 °C), 30 cycles of denaturation (15 s, 95 °C) annealing/extension (60 s, 60 °C). Genotype determination was made in Bio-Rad CFX96 system (BioRad, CA, USA).
Galita G., Sarnik J., Brzezinska O., Budlewski T., Dragan G., Poplawska M., Majsterek I., Poplawski T, & Makowska J.S. (2023). Polymorphisms in DNA Repair Genes and Association with Rheumatoid Arthritis in a Pilot Study on a Central European Population. International Journal of Molecular Sciences, 24(4), 3804.
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Publication 2023
Adjustment Disorders Biological Assay EXO1 protein, human Genetic Diversity Genotype MBD4 protein, human MRE11 protein, human MUTYH protein, human Neutrophil OGG1 protein, human Oligonucleotide Primers PRKDC protein, human RAD52 protein, human SMUG1 protein, human TP53 protein, human XRCC1 protein, human XRCC2 protein, human XRCC3 protein, human XRCC5 protein, human
4
Dietary Intervention for FAP Patients

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Publication 2023
Anti-Inflammatory Agents Anti-Inflammatory Agents, Non-Steroidal Anus Aspirin Cardiovascular Diseases Child Colectomy Colon Curcumin Diarrhea Dietary Supplements Fibromatosis, Aggressive Fibrosis Gastroenterologist Ileal Pouch Anal Anastomosis Ileum Intestines Investigational New Drugs Males Malignant Neoplasms Microbial Community Mutation MUTYH protein, human Operative Surgical Procedures Ostomy Patients Pharmaceutical Preparations Polyps Probiotics Proctocolectomy Proctosigmoidoscopy Rectum Surgical Anastomoses Surgical Stoma Tumeric Voluntary Workers
5
Germline Genetic Testing for Cancer
Germline genetic testing costs were covered by institutional research study funds and by foundational grants. Genetic testing was performed on the saliva sample via the clinical Color Genomics targeted panel of 30 cancer predisposition genes: APC, ATM, BAP1, BARD1, BMPR1A, BRCA1, BRCA2, BRIP1, CDH1, CDK4, CDKN2A(p14ARF), CDKN2A (p16INK4a), CHEK2, EPCAM, GREM1, MITF, MLH1, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, POLD1, POLE, PTEN, RAD51C, RAD51D, SMAD4, STK11, and TP53.
Cheng H.H., Sokolova A.O., Gulati R., Bowen D., Knerr S.A., Klemfuss N., Grivas P., Hsieh A., Lee J.K., Schweizer M.T., Yezefski T., Zhou A., Yu E.Y., Nelson P.S, & Montgomery B. (2023). Internet-Based Germline Genetic Testing for Men With Metastatic Prostate Cancer. JCO Precision Oncology, 7, e2200104.
Publication 2023
BMPR1A protein, human BRCA1 protein, human CDH1 protein, human CDKN2A Gene CHEK2 protein, human Gene, BRCA2 Gene, Cancer Germ Line GREM1 protein, human MITF protein, human MLH1 protein, human MSH6 protein, human MUTYH protein, human Oncogenes p14ARF Protein PALB2 protein, human PMS2 protein, human POLD1 protein, human PTEN protein, human RAD51C protein, human Saliva SMAD4 protein, human STK11 protein, human Susceptibility, Disease TACSTD1 protein, human TP53 protein, human

Top products related to «MUTYH protein, human»

1
Qiaamp dna blood mini kit by Qiagen
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Mutyh by Abcam
MUTYH is a DNA glycosylase enzyme that is involved in the base excision repair pathway. It is responsible for the removal of adenine and 2-hydroxyadenine from DNA, helping to maintain genomic integrity.
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2100 bioanalyzer by Agilent Technologies
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More about "MUTYH protein, human"

The MUTYH gene encodes a DNA glycosylase enzyme that plays a crucial role in the base excision repair (BER) pathway.
This enzyme is responsible for the removal of 8-oxoguanine, a mutagenic DNA lesion caused by oxidative stress, from the genome.
By preventing the accumulation of G:C to T:A transversions, MUTYH helps maintain genomic integrity and safeguard against the development of oncogenic mutations.
MUTYH-associated polyposis (MAP) is an autosomal recessive disorder characterized by the formation of multiple colorectal adenomas and an elevated risk of colorectal cancer.
Researchers studying the MUTYH protein can leverage powerful tools like PubCompare.ai, an AI-driven platform, to optimize their research protocols, enhance reproducibility, and locate the best protocols from the literature, preprints, and patents.
To study the MUTYH protein, researchers may utilize techniques such as the QIAamp DNA Blood Mini Kit for DNA extraction, the HiSeq 2000 or HiSeq 2500 platforms for high-throughput sequencing, and the High-Capacity cDNA Reverse Transcription Kit for gene expression analysis.
Microscopic imaging using a DMi8b fluorescent microscope and the MiSeq platform for targeted sequencing may also be employed.
Additionally, researchers may utilize TaqMan SNP Genotyping Assays to detect specific genetic variants and the 2100 Bioanalyzer for quality control of nucleic acid samples.
By incorporating these techniques and tools, researchers can gain deeper insights into the function and regulation of the MUTYH protein, ultimately advancing our understanding of its role in DNA repair and its implications for cancer prevention and treatment.
The wealth of available resources and the power of AI-driven platforms like PubCompare.ai can help streamline and optimize MUTYH protein research, leading to more reliable and impactful findings.