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GREM1 protein, human

GREM1 (Gremlin-1) is a secreted antagonist of bone morphogenetic proteins (BMPs) that plays a key role in regulating cell growth, differentiation, and development.
It is involved in various physiological and pathological processes, including embryonic patterning, tissue repair, and the progression of certain diseases.
Researching GREM1 protein functions and interactions can provide valuable insights into these complex biological systems.
PubCompare.ai offers an AI-driven platform to optimize your GREM1 investigations by locating the best protocols from literature, preprints, and patents, using intelligent comparisons to enhance reproducibility and accuaracy.
Streamline your GREM1 research with the power of PubCompare.ai's advanced tools and analytics, and experience the future of scientific discovery today.

Most cited protocols related to «GREM1 protein, human»

Both MGPT and TP53 gene-specific tests were performed from DNA isolated from whole blood or saliva samples. NGS analysis (Illumina, San Diego, CA) was performed in all coding domains plus at least five bases into the 5′ and 3′ ends of the introns and untranslated regions (5′UTR and 3′UTR) for all cancer susceptibility genes. EPCAM and GREM1 were only analyzed for gross deletions and duplications, if included on the panel. Depending on the panel ordered by the clinician, 5–49 genes, including TP53, were analyzed. Sanger sequencing was performed for any region with insufficient depth of coverage (<10X), for verification of all variants (other than known benign variants), and for those with decreased mutant to wild-type allele ratios. A targeted chromosomal microarray and/or MLPA was used for the detection of gross deletions and duplications.
A five-tier classification schema—pathogenic; variant, likely pathogenic; variant of unknown significance; variant, likely benign; and benign—was used to classify variants.29 (link)
Publication 2017
3' Untranslated Regions 5' Untranslated Regions Alleles BLOOD Chromosomes Gene, Cancer Gene Deletion Genes Genetic Testing GREM1 protein, human Introns Microarray Analysis Multiplex Ligation-Dependent Probe Amplification Pathogenicity Saliva Susceptibility, Disease TACSTD1 protein, human TP53 protein, human Untranslated Regions

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Publication 2014
ACTA2 protein, human Adult Animals, Transgenic Arm, Upper Bone Marrow Clone Cells Exons GREM1 protein, human Intestines LacZ Genes Oligonucleotide Primers Protein Biosynthesis Recombination, Genetic Tamoxifen tdTomato

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Publication 2019
Actins Anti-Antibodies APEX1 protein, human Buffers Cells Glycine Goat GREM1 protein, human Histone H3 Hyperostosis, Diffuse Idiopathic Skeletal Hypoxia Immunoglobulins Mus Nitrocellulose NOX4 protein, human Proliferating Cell Nuclear Antigen Proteins Rabbits RNA, Small Interfering SDS-PAGE Serum Technique, Dilution Tissue, Membrane Tissues Tromethamine Vision Western Blotting
Laboratory procedures were performed at the Color laboratory (Burlingame, CA) under Clinical Laboratory Improvements Amendments (#05D2081492) and College of American Pathologists (#8975161) compliance as previously described (3 (link)). Briefly, genomic DNA was extracted from blood or saliva (Perkin Elmer Chemagic DNA Extraction Kit), enriched for select regions using SureSelect XT probes and then sequenced using NextSeq 500/550 or NovaSeq 6000 instruments (Illumina). Sequence reads were aligned against human genome reference GRCh37.p12 with the Burrows–Wheeler Aligner (13 ), and duplicate and low quality reads were removed. Single nucleotide variants and small insertions and deletions (indels, 2–50 bp) were called by the HaplotypeCaller module of GATK3.4 (14 (link)). Variants in homopolymer regions were called by an internally developed algorithm using SAMtools. Large structural variants (>50 bp) were detected using dedicated algorithms based on read depth (CNVkit) (15 (link)), paired reads and split reads [LUMPY (16 (link)), in-house developed algorithms].
Variants were classified according to the standards and guidelines for sequence variant interpretation of the American College of Medical Genetics and Genomics (17 (link)), and all variant classifications were signed out by board certified medical geneticist or pathologist. Variant classification categories are pathogenic (P), likely pathogenic (LP), variant of uncertain significance (VUS), likely benign (LB) and benign (B).
The genes in Color Data were selected based on (i) published evidence of their association with hereditary cancer risk and (ii) the technical feasibility of sequencing them using the NGS methods described above. These genes are APC, ATM, BAP1, BARD1, BMPR1A, BRCA1, BRCA2, BRIP1, CDH1, CDK4, CDKN2A (p14ARF and p16INK4a), CHEK2, EPCAM, GREM1, MITF, MLH1, MSH2, MSH6, MUTYH, NBN, PALB2, PMS2, POLD1, POLE, PTEN, RAD51C, RAD51D, SMAD4, STK11 and TP53. Analysis, variant calling and reporting focused on the complete coding sequence and adjacent intronic sequence of the primary transcript(s) (Table S1), unless otherwise indicated. In PMS2, exons 12–15 were not analyzed. In several genes, only specific positions known to impact cancer risk were analyzed (genomic coordinates in GRCh37): CDK4—only chr12:g.58145429-58145431 (codon 24), MITF—only chr3:g.70014091 (including c.952G>A), POLD1—only chr19:g.50909713 (including c.1433G>A), POLE—only chr12:g.133250250 (including c.1270C>G), EPCAM—only large deletions and duplications including the 3′ end of the gene and GREM1—only duplications in the upstream regulatory region.
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Publication 2019
BLOOD BMPR1A protein, human BRCA1 protein, human CDH1 protein, human CDKN2A Gene CHEK2 protein, human Clinical Laboratory Services Codon Exons Gene, BRCA2 Gene Deletion Genes Genome Genome, Human GREM1 protein, human INDEL Mutation Insertion Mutation Introns Malignant Neoplasms MITF protein, human MLH1 protein, human MSH6 protein, human Multiple Birth Offspring MUTYH protein, human Nucleotides Open Reading Frames PALB2 protein, human Pathogenicity Pathologists PMS2 protein, human POLD1 protein, human PTEN protein, human RAD51C protein, human Regulatory Sequences, Nucleic Acid Saliva SMAD4 protein, human STK11 protein, human TACSTD1 protein, human TP53 protein, human
In the replication stage, we meta-analyzed results from: (1) individuals of European descent only (Rep-EUR); and (2) all replication cohorts with multiple ethnicities (Rep-All). Likewise we meta-analyzed results from discovery cohorts and European-descent-only replication cohorts (“Combined EUR”) from discovery cohorts and all replication cohorts (“Combined All”). To investigate and account for potential heterogeneities in allelic effects between studies, we also performed “trans-ethnic meta-analysis” using MANTRA25 (link) in the replication sample that included all ethnic groups (“Rep-All”) and in the combined analysis of the discovery and all ethnic groups in the replication sample (“Combined All”).
A successful replication was considered if: (1) the association p-value in the cumulative-meta-analysis (Combined EUR) was genome-wide significant (p < 5 × 10−8) and less than the discovery meta-analysis p-value; or (2) the association p-value in the meta-analysis of replication-cohorts only (Rep-EUR) was less than p = 0.0024 (a Bonferroni-adjusted threshold at p = 0.05/21 since there were a total of 21 tests performed for whole body and appendicular lean mass in Rep-EUR cohorts during replication). Using the METAL package we also estimated I2 to quantify heterogeneity and p-values to assess statistical significance for a total of eight associations that were replicated in the cumulative-meta-analysis (combined EUR, five SNPs for whole body and three for appendicular lean mass).
To estimate the phenotypic variance explained by the genotyped SNPs in the Framingham Heart Study (FHS), we used a restricted maximum likelihood model implemented in the GCTA (Genome-wide Complex Trait Analysis) tool package57 (link), 58 (link) and adjusted for the same set of covariates included in our GWAS.
Finally, we examined associations between all imputed SNPs in/near five genes (THRH, GLYAT, GREM1, CNTF, and PRDM16 including 60 kB up and downstream of the gene) and lean mass, as these genes have been implicated to have associations with lean mass in previous association studies18 (link)–20 (link).
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Publication 2017
Alleles Ciliary Neurotrophic Factor DNA Replication Ethnic Groups Ethnicity Europeans Genes Genetic Heterogeneity Genome Genome-Wide Association Study GREM1 protein, human Human Body MEL1S protein, human Metals Phenotype Polygenic Traits Single Nucleotide Polymorphism

Most recents protocols related to «GREM1 protein, human»

The PBMSCs (80%-90% confluency) were digested with 0.25% trypsin containing EDTA and inoculated into six-well plates at a cell density of 2 × 104 cells/cm2. The differentiated PBMSCs were transfected with si-circRNA-ACCHC14, oe-circRNA-ACCHC143, si-GREM1, oe-GREM1, si-BMP2, oe-BMP2, miR-181a mimic, miR-181a inhibitor or their negative controls using Lipofectamine 2000 transfection reagent (Invitrogen, Carlsbad, CA, USA). After transfection, the cells were cultured in an incubator at 37 °C with 5% CO2 for 48 h.
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Publication 2023
BMP2 protein, human Cells Edetic Acid GREM1 protein, human lipofectamine 2000 RNA, Circular Transfection Trypsin
Genomic deoxyribonucleic acid was extracted from paraffin embedded tissue using GeneJET Genomic deoxyribonucleic acid Purification Kit (ThermoScientific), according to manufacturer protocol. SNPs polymorphisms of the TCF7L2 (rs7903146, C/T), cancer susceptibility 21 (rs6983267, G/T), and GREM1 (rs1696981, C/T) were identified using a real-time PCR method based on the TaqMan® Genotyping Master Mix (Applied Biosystems) and 20× SNP Genotyping Assay (Applied Biosystems), using a 7500 Fast Real-Time Systems (Applied Biosystems) according to manufacturer procedure. Allelic discrimination was made with the help of 7500 Fast Real-Time PCR software, version 2.3.
Publication 2023
Alleles Biological Assay Discrimination, Psychology DNA Genetic Polymorphism Genome GREM1 protein, human Malignant Neoplasms Paraffin Embedding Real-Time Polymerase Chain Reaction Susceptibility, Disease TCF7L2 protein, human Tissues
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.
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
Genetic testing was performed in a Clinical Laboratory Improvement Amendments– and College of American Pathology–approved laboratory (Myriad Genetic Laboratories Inc, Salt Lake City, UT). The hereditary cancer panel was composed of 25-35 cancer-associated genes; the initial multigene panel test included 25 genes (APC, ATM, BARD1, BMPR1A, BRCA1, BRCA2, BRIP1, CDH1, CDK4, CHEK2, MLH2, MSH2, MSH6, MUTYH, NBN, P14ARF, P16, PALB2, PMS2, PTEN, RAD51C, RAD51D, SMAD4, STK11, and TP53). Subsequent additions to the panel test in 2016 and 2019 included GREM1, HOXB13, POLD1, POLE, AXIN2, GALNT12, MSH3, NTHL1, RNF43, and RPS20. This next-generation sequencing assay has been detailed previously.15 (link),16 (link) Sequencing and large rearrangement analysis was performed for all genes evaluated except HOXB13, POLD1, and POLE, for which only sequencing is performed, and EPCAM and GREM1, in which only large rearrangement analysis is performed.
Variant classification was performed using the American College of Molecular Genetics and Genomics and Association for Molecular Pathology guidelines, as well as previously described statistical variant classification methods.17 (link)-20 (link) Variants with a laboratory classification of deleterious or suspected deleterious were considered pathogenic.
Publication 2023
AXIN2 protein, human Biological Assay BMPR1A protein, human BRCA1 protein, human CDH1 protein, human CHEK2 protein, human Clinical Laboratory Services Gene, BRCA2 Gene, Cancer Genes GREM1 protein, human HOXB13 protein, human Malignant Neoplasms mismatch repair protein 1, human MSH6 protein, human MUTYH protein, human NTHL1 protein, human Oncogenes PALB2 protein, human Pathogenicity PMS2 protein, human POLD1 protein, human PTEN protein, human RAD51C protein, human Reproduction RPS20 protein, human Salts SMAD4 protein, human STK11 protein, human TACSTD1 protein, human TP53 protein, human
The index patient originated from the EX2TRICAN project, proposing ES in extreme cancer phenotypes using different strategies: (i) trio ES for early onset sporadic cases or sporadic cases with multiple primary malignancies for comparative index case-parents ES strategy, originally developed to detect de novo variants; (ii) ES of two distant cases in families with a strong aggregation of cancer cases; (iii) solo ES with familial segregation of candidate variants for very rare cancer types or if only the proband is available for ES. Among patients included in this study, there were 3 patients from families with multiple cases of MBC.
In order to give emphasis of the possible role of ATR in the predisposition to BC and in particular MBC, we constituted a replication cohort of 86 MBC cases, 28 MBC related women and 47 women with very high risk of BC according to the BOADICEA software [52 (link)]. Patients with MBC have been recruited from Dijon University Hospital, the anti-cancer Center Georges François Leclerc (CGFL Dijon) and a national collaboration call, and the MBC related women and women with very high risk of BC families have been recruited from Dijon University Hospital and the CGFL Dijon. All patients of this cohort have been tested negatively at least for the more penetrant BC predisposition genes (BRCA1, BRCA2 and PALB2).
Finally, after the discovery of the first ATR variant by ES, ATR has been included in the cancer gene-panel used for genetic predisposition to cancer at CGFL Dijon. This lead to the identification of two ATR variants in patients PED9545.1 and PED7847.1. They were negative for the following predisposition genes : BRCA1, BRCA2, PALB2, PTEN, TP53, RAD51C, RAD51D, CDH1, EPCAM, MLH1, MSH2, MSH6, PMS2, APC, MUTYH, AXIN2, GREM1, NTHL1, POLD1, POLE, SMAD4, STK11, RET, MEN1, SDHAF2, SDHB, SDHC, SDHD, VHL, FLCN, WT1, BAP1, CDKN2A, CDK4, PRSS1, NF1, PTCH1, PTCH2.
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Publication 2023
AXIN2 protein, human BRCA1 protein, human CDH1 protein, human CDKN2A Gene DNA Replication FLCN protein, human Gene, BRCA2 Gene, Cancer Genetic Predisposition to Disease GREM1 protein, human Malignant Neoplasms MLH1 protein, human MSH6 protein, human Multiple Endocrine Neoplasia Type 1 MUTYH protein, human NTHL1 protein, human PALB2 protein, human Parent Patients Phenotype PMS2 protein, human POLD1 protein, human PRSS1 protein, human PTCH1 protein, human PTCH2 protein, human PTEN protein, human RAD51C protein, human SDHB protein, human SDHC protein, human SMAD4 protein, human STK11 protein, human Susceptibility, Disease TACSTD1 protein, human TP53 protein, human TRIO protein, human Woman

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More about "GREM1 protein, human"

Gremlin-1 (GREM1) is a secreted protein that acts as an antagonist of bone morphogenetic proteins (BMPs), playing a crucial role in regulating cell growth, differentiation, and development.
This versatile protein is involved in various physiological and pathological processes, including embryonic patterning, tissue repair, and the progression of certain diseases.
Researching the functions and interactions of the GREM1 protein can provide valuable insights into complex biological systems.
Streamlining your GREM1 investigations with the power of PubCompare.ai's advanced tools and analytics can enhance the reproducibility and accuracy of your research.
This AI-driven platform helps you locate the best protocols from literature, preprints, and patents, using intelligent comparisons to optimize your experimental design.
To further support your GREM1 research, consider using tools like Lipofectamine 2000 for efficient gene transfection, TRIzol reagent and RNeasy Mini Kit for RNA extraction and purification, and the High-Capacity cDNA Reverse Transcription Kit for complementary DNA synthesis.
Additionally, Matrigel, a complex extracellular matrix, can be used to study GREM1's role in cell-matrix interactions, while FBS and Polybrene can enhance cell culture and viral transduction, respectively.
Unlock the full potential of your GREM1 investigations by leveraging the latest advancements in scientific research, including the powerful AI-driven platform offered by PubCompare.ai.
Experience the future of scientific discovery today and gain valuable insights into the complex biological processes regulated by this fascinating protein.