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COL1A2 protein, human

COL1A2 is a gene that provides instructions for making one of the two main components of type I collagen, a protein that is the most abundant in the human body.
Type I collagen is a major structural component of skin, bone, teeth, and connective tissues.
Mutations in the COL1A2 gene can lead to genetic disorders affecting collagen, such as osteogenesis imperfecta and Ehlers-Danlos syndrome.
Understanding the role of COL1A2 and its related pathways is crucial for researching and developing treatments for these conditions.
Discover cutting-edge protocols and leverage AI-driven comparisons to optimize your COL1A2 protein research with PubCompare.ai's intuitive platfrom - experiance the future of scientific discovery today.

Most cited protocols related to «COL1A2 protein, human»

1
Computational Annotation of Immune and Non-Immune Cell Transcriptomes from Tumor Tissues
Cited 19 times

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Publication 2019
ACTA2 protein, human CDH5 protein, human Cells COL1A2 protein, human Endothelial Cells Epithelial Cells Fibroblasts Gene Expression Genes Goblet Cells Homo sapiens KRT5 protein, human Neoplasms Patients PTPRC protein, human secretion TACSTD1 protein, human Tissues Transcriptome
2
Annotation of Immune Cell Clusters
Cited 16 times
Clusters were annotated based on expression of known marker genes, including CD3G, CD3D, CD3E, CD2 (T cells), CD8A, GZMA (CD8+ T cells), CD4, FOXP3 (CD4+ T cells/Tregs), KLRC1, KLRC3 (NK cells), CD19, CD79A (B cells), SLAMF7, IGKC (Plasma cells), FCGR2A, CSF1R (Macrophages), FLT3 (Dendritic cells), CLEC4C (Plasmacytoid Dendritic cells), COL1A2 (Fibroblasts), MCAM, MYLK (Myofibroblasts), FAP, PDPN (CAFs), EPCAM, TP63 (Malignant cells), PECAM1, VWF (Endothelial cells), PMEL, MLANA (Melanocytes). Clusters were also confirmed by identifying differentially expressed marker genes for each cluster and comparing to known cell type marker genes. Finally, we downloaded bulk RNA-seq count data from sorted immune cell populations from Calderon et al., 20186 (link) and compared bulk gene expression to pseudo-bulk expression profiles from single cell clusters. UMI counts were summed for all cells in each cluster to generate pseudo-bulk profiles. Gene counts from aggregated single-cell and bulk data were then normalized and depth corrected using variance stabilizing transformation in DESeq2 (version 1.18.1). Genes with a coefficient of variation greater than 20% across bulk RNA-seq datasets were used to calculate the Pearson correlation between bulk datasets and pseudo-bulk profiles.
Yost K.E., Satpathy A.T., Wells D.K., Qi Y., Wang C., Kageyama R., McNamara K., Granja J.M., Sarin K.Y., Brown R.A., Gupta R.K., Curtis C., Bucktrout S.L., Davis M.M., Chang A.L, & Chang H.Y. (2019). Clonal replacement of tumor-specific T cells following PD-1 blockade. Nature medicine, 25(8), 1251-1259.
Publication 2019
B-Lymphocytes CD4 Positive T Lymphocytes CD8-Positive T-Lymphocytes CD31 Antigens CD79A protein, human Cells COL1A2 protein, human Conotruncal Anomaly Face Syndrome Dendritic Cells Dietary Fiber Endothelial Cells FCGR2A protein, human Fibroblasts FLT3 protein, human Gene, c-fms Gene Expression Genes Genetic Markers GZMA protein, human Macrophage MCAM protein, human Melanocyte MLANA protein, human MYLK protein, human Myofibroblasts Natural Killer Cells Plasma Cells Plasmacytoid Dendritic Cells Population Group RNA-Seq SILV protein, human SLAMF7 protein, human T-Lymphocyte TACSTD1 protein, human TP63 protein, human
3
Compartment-based Gene Expression Analysis
Cited 12 times

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Publication 2019
CD79A protein, human CD79B protein, human CDH5 protein, human Cells Cell Separation COL1A2 protein, human Epithelial Cells Gene, c-fms Gene Expression Genes KRT8 protein, human KRT18 protein, human Stromal Cells TACSTD1 protein, human
4
Generation and Characterization of G610C OI Mice
Cited 10 times
Knock-in mice were created using embryonic stem cells and Cre/lox P technology. A 13 kb genomic clone containing the relevant segment of the murine Col1a2 gene was isolated from a λ phage library constructed with gDNA of the 129Sv/Ev Taconic mouse strain. PCR site-directed mutagenesis was used to change the targeted codon from GGT to TGT. The Col1a2 G610C-positive embryonic stem cells were injected into blastocysts of C57BL/6J (B6) mice. Founder mice that retain the neo targeting vector are termed neo+ or G610C Neo mice. Progeny obtained by breeding a founder male with a female that expressed Cre recombinase (Jackson Laboratory, Bar Harbor, ME, USA, Stock Number 003724) are termed neo– or G610C OI mice. The G610C OI mouse line is available to the research community through the Jackson Laboratory Mouse Repository (Jax Stock Number: 007248).
Four F1 strains of G610C OI mice were used to determine the effect of genetic background on phenotype in 2-month-old male mice. Incipient congenic G610C OI B6 (∼98% B6 genetic background) male breeders were generated by six generations of backcrosses to Jackson Laboratory B6 mice (Stock Number 000664). Experimental heterozygous B6 male breeders were crossed with A/J (Stock Number 000646), BALB/cByJ (Stock Number 001026), C3H/HeJ (Stock Number 000659), and FVB/NJ (Stock Number 001806) females purchased from the Jackson Laboratory. Progeny of these crosses are designated, respectively, as A.B6, Cby.B6, C3.B6, and FVB.B6. Experimental mice were housed at UMB in a single specific-pathogen-free room and were exposed to identical environmental conditions consisting of a 12 hour light/dark cycle, an ambient temperature of 23°C, and ad libitum access to water and laboratory mouse chow. Genotype was assigned using a PCR assay that can discriminate the three possible G610C OI mouse genotypes. The forward primer (TCC CTG CTT GCC CTA GTC CCA AAG ATC CTT) and the reverse primer (AAG GTA TAG ATC AGA CAG CTG GCA CAT CCA) will generate a 165 bp (wild type) or a 337 and a 165 bp (heterozygous) or a 337 bp (homozygous) PCR product using G610C OI mice gDNA. All animals were euthanized by CO2 asphyxiation.
Daley E., Streeten E.A., Sorkin J.D., Kuznetsova N., Shapses S.A., Carleton S.M., Shuldiner A.R., Marini J.C., Phillips C.L., Goldstein S.A., Leikin S, & McBride DJ J.r. (2009). Variable Bone Fragility Associated With an Amish COL1A2 Variant and a Knock-in Mouse Model. Journal of Bone and Mineral Research, 25(2), 247-261.
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Publication 2009
Animals Asphyxia Bacteriophages Biological Assay Blastocyst Clone Cells Cloning Vectors Codon COL1A2 protein, human Cre recombinase DNA Library Embryonic Stem Cells Females Genes Genetic Background Genome Genotype Heterozygote Homozygote Males Mice, House Mice, Laboratory Mus Mutagenesis, Site-Directed Oligonucleotide Primers Phenotype Specific Pathogen Free Strains
5
Multiplex Fluorescent In Situ Hybridization
Cited 9 times
Samples were fixed in either 10% neutral buffered formalin, dehydrated with ethanol and embedded in paraffin wax or fixed in 4% paraformaldehyde and embedded in OCT compound. Sections from paraffin (5 μm) and OCT (20 μm) blocks were processed using standard pre-treatment conditions for each per the RNAscope multiplex fluorescent reagent kit version 2 (Advanced Cell Diagnostics) assay protocol. TSA-plus fluorescein, Cy3 and Cy5 fluorophores were used at 1:500 dilution. Micrographs were acquired with a laser scanning confocal fluorescence microscope (Zeiss LSM780) and processed with ImageJ and Imaris (version 9.2.0, Oxford Instruments). smFISH experiments were performed on at least 2 human or mouse subjects distinct from the donors used for sequencing, and quantifications were based on at least 10 fields of view in each. For smFISH, fields of view were scored manually, calling a cell positive for each gene probed if its nucleus had >3 associated expression puncta. Proprietary (Advanced Cell Diagnostics) probes used were: KRT5 (547901-C2), SERPINB3 (828601-C3), SFTPC (452561-C2), WIF1 (429391), CLDN5 (517141-C2, 517141-C3), MYC (311761-C3), ACKR1 (525131, 525131-C2), COL1A2 (432721), GPC3 (418091-C2), SERPINF1 (564391-C3), C20rf85 (560841-C3), DHRS9 (467261), GJA5 (471431), CCL21 (474371-C2), COX4I2 (570351-C3), APOE (433091-C2), ACGT2 (828611-C2), ASPN (404481), IGSF21 (572181-C3), GPR34 (521021), EREG (313081), GPR183 (458801-C2), TREM2 (420491-C3), CHI3L1 (408121), MYRF (499261), AGER (470121-C3), TBX5 (564041), KCNK3 (536851), ACVRL1 (559221), SERPINA1 (435441), HHIP (464811), Slc7a10 (497081-C2), Fgfr4 (443511), Pi16 (451311-C2), Serpinf1 (310731), Hhip (448441-C3), Sftpc (314101-C2), Nkx2–1 (434721-C3), and Myrf (524061).
Travaglini K.J., Nabhan A.N., Penland L., Sinha R., Gillich A., Sit R.V., Chang S., Conley S.D., Mori Y., Seita J., Berry G.J., Shrager J.B., Metzger R.J., Kuo C.S., Neff N., Weissman I.L., Quake S.R, & Krasnow M.A. (2020). A molecular cell atlas of the human lung from single cell RNA sequencing. Nature, 587(7835), 619-625.
Publication 2020
ACVRL1 protein, human ApoE protein, human Biological Assay CCL21 protein, human Cell Nucleus Cells COL1A2 protein, human DARC protein, human Diagnosis Donors EREG protein, human Ethanol FGFR4 protein, human Fluorescein Fluorescence Formalin Genes GPC3 protein, human HHIP protein, human Homo sapiens KRT5 protein, human Microscopy, Confocal Mus NKX2-1 protein, human Paraffin paraform RAGE receptor protein, human SERPINA1 protein, human SERPINB3 protein, human Technique, Dilution TREM2 protein, human

Most recents protocols related to «COL1A2 protein, human»

1
Expression Analysis of Chl1 in Intestinal Cell Populations
Not available on PMC !

Example 2

Next, the expression of Chl1 was confirmed using various tissues or cells.

(B) The intestinal epithelium (EpCAM-positive CD45-negative), fibroblasts (COL1a2-GFP-positive CD45-negative podoplanin-positive), macrophages (F480-positive CD11b-positive), CD4-positive T cells, B cells (CD19-positive B220-positive), and lamina propria cells of the large intestine (whole colon cells) were isolated in the same way as above. RNA was purified from each cell using TRIZOL (Thermo Fisher Scientific Inc./Invitrogen: 15596018) and subsequently reverse-transcribed using VILO (Thermo Fisher Scientific Inc./Invitrogen: 11755500). The expression analysis of Chl1 was conducted using Universal Probe Library (Roche Life Science) and LightCycler™ 480 system (Roche Life Science). Comparison with the expression of Gapdh is shown (n=3). The results were as shown in FIG. 2.

As shown in FIG. 2, Chl1 exhibited high expression in fibroblasts, particularly, fibroblasts at the acute phase (“Acute”) and chronic phase “Chronic” of induced inflammation. This suggested that Chl1 may be preferably used as a marker for acute and chronic inflammation.

US11866497B2. Antibody to fibrosis-related molecule and medical application thereof (2024-01-09). The University of Tokyo [JP]. Inventors: Yosuke Kurashima [JP], Hiroshi Kiyono [JP].
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Patent 2024
B-Lymphocytes CD4 Positive T Lymphocytes cDNA Library Cells COL1A2 protein, human Colon Fibroblasts GAPDH protein, human Inflammation Intestinal Epithelium ITGAM protein, human Lamina Propria Large Intestine Macrophage TACSTD1 protein, human Tissues trizol
2
Comprehensive Transcriptomic Analysis of Hepatocellular Carcinoma
The following bulk RNA-sequencing expression profiles and corresponding clinical data were downloaded from the TCGA database (https://portal.gdc.comn = 377). Raw sequencing reads were aligned using the STAR aligner and expressed as fragments per million mapped reads (FPKM). Gene expression profiles were standardized using R (https://www.r-project.org/). Only patients with complete clinical information related to the analysis were retained. Training and testing groups were randomly assigned in a ratio of 1:1 among the patients. To establish an independent validation cohort, Clinical pathology and RNA-Seq mRNA expression data were obtained for 232 samples from the ICGC portal (https://dcc.icgc.org/projects/LIRI-JP). The UCSC Xena server was used to retrieve somatic mutations and methylation data for HCC (https://xenabrowser.net/). The GEO database was used to download data for single-cell RNA sequencing of primary HCC tissues (GSE149614, n = 10). “Seurat” and “NormalizeData” R packages were used for the standardization of the single-cell RNA-Seq data. “FingVariableGenes” R package was used for the identification of the top 3,000 highly variable genes. The determination of cell types was as shown in Supplementary Figure S1A (Malignant cell markers-GPC3, CD24, MDK, KRT18; Meyloid cell markers-CD68, AIF1, C1QA, TPSAB1; T cell markers-CD3D, CD3E, CD2; B cell markers-MZB1, MS4A1, CD79A; Fibroblast cell markers-COL1A2, COL3A1, ACTA2; Endothelial cell markers-FLT1, RAMP2, PLVAP).
Ma Y.L., Yang Y.F., Wang H.C., Yang C.C., Yan L.J., Ding Z.N., Tian B.W., Liu H., Xue J.S., Han C.L., Tan S.Y., Hong J.G., Yan Y.C., Mao X.C., Wang D.X, & Li T. (2023). A novel prognostic scoring model based on copper homeostasis and cuproptosis which indicates changes in tumor microenvironment and affects treatment response. Frontiers in Pharmacology, 14, 1101749.
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Publication 2023
ACTA2 protein, human B-Lymphocytes CD79A protein, human Cells COL1A2 protein, human Dietary Fiber Diploid Cell Endothelial Cells Fibroblasts FLT1 protein, human Genes GPC3 protein, human KRT18 protein, human Methylation Mutation Patients RNA, Messenger Single-Cell RNA-Seq T-Lymphocyte Tissues Transcription, Genetic
3
Western Blot Analysis of Lung Proteins
Snap frozen lung lobes or cells were lysed in RIPA buffer with a protease inhibitor cocktail, and the protein concentrations were measured by Pierce BCA Assay Kit (Cat#: 23227, Thermo Fisher Scientific). A total 20 µg protein for each sample was used for analysis. The protein samples were separated by 10% sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE), and then transferred to a nitrocellulose membrane (Cat# 1620112, BioRad). The membranes were then blocked with EveryBlot Blocking Buffer (Cat#: 12010020, BioRad) for 20 min, and incubated with primary antibody diluted in blocking buffer overnight at 4 °C. Primary antibodies used here included anti-REV-ERBα (1:1000, 13418, Cell Signaling), anti-COL4A1 (1:1000, ab227616, Abcam), anti-LOXL2 (1:1000, ab197779, Abcam), anti-E-Cadherin (1:1000, 3195, Cell Signaling), anti-Fibronectin (1:1000, ab, Abcam), anti-vimentin (1:1000, ab92547, Abcam); anti-COL1A2 (1:1000, NBP2-92790, Novus Biologicals), anti-COL1A1 (1:1000, NBP1-30054, Novus Biologicals), anti-activated LOX (1:1000, NB100-2527, Novus Biologicals) for Fig. 7 only, and anti-LOX (1:1000, ab174316, abcam). Then, the primary antibody was removed, and the membranes were washed with Tris-buffered saline containing 0.1% Tween 20 (TBS-T) 3 times, 10 min each. Then, membranes were incubated with secondary antibody (goat-anti-rabbit, 1:5000, #1706515, BioRad) for 1 h at room temperature. The membranes were then washed with TBS-T 4 times, 15 min each. The membranes were developed with Pierce ECL Western Blotting Substrate (Cat#: 32106, Thermo Scientific), and the signals were detected by Bio-Rad ChemiDoc MP imaging system Densitometry was calculated using ImageLab software (BioRad), and fold changes were calculated based on PBS groups, with normalization to β-actin (1:2500, ab20272, Abcam) for mice and GAPDH (1:1000, ab9482, Abcam) for human samples.
Wang Q., Sundar I.K., Lucas J.H., Park J.G., Nogales A., Martinez-Sobrido L, & Rahman I. (2023). Circadian clock molecule REV-ERBα regulates lung fibrotic progression through collagen stabilization. Nature Communications, 14, 1295.
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Publication 2023
Actins Antibodies Biological Assay Biological Factors Buffers Cells COL1A2 protein, human Densitometry E-Cadherin Fibronectins Freezing GAPDH protein, human Goat Homo sapiens Immunoglobulins LOXL2 protein, human Lung Mus Nitrocellulose Novus Protease Inhibitors Proteins Rabbits Radioimmunoprecipitation Assay Saline Solution SDS-PAGE Staphylococcal Protein A Tissue, Membrane Tween 20 Vimentin
4
Collagen Phenotyping in Melanoma
We summarized data on collagen molecules from The Human Genome Organisation (HUGO) portal: COL1A1, COL1A2, COL2A1, COL3A1, COL4A1, COL4A2, COL4A3, COL4A4, COL4A5, COL4A6, COL5A1, COL5A2, COL5A3, COL6A1, COL6A2, COL6A3, COL6A5, COL6A6, COL7A1, COL8A1, COL8A2, COL9A1, COL9A2, COL9A3, COL10A1, COL11A1, COL11A2, COL12A1, COL13A1, COL14A1, COL15A1, COL16A1, COL17A1, COL18A1, COL19A1, COL20A1, COL21A1, COL22A1, COL23A1, COL24A1, COL25A1, COL26A1, COL27A1, and COL28A1. First, based on the expression level of 44 collagen molecules, unsupervised clustering analysis was used to identify the collagen phenotypes in melanoma, to classify patients. The optimal clustering number of melanoma-Cohort was determined by the consensus clustering algorithm, and its stability was verified. The R package “ConsensusClusterPlus” was used to perform each step, and the process was repeated 50 times (resampling rate 80%).34 (link)
Sha Y., Mao A.Q., Liu Y.J., Li J.P., Gong Y.T., Xiao D., Huang J., Gao Y.W., Wu M.Y, & Shen H. (2023). Nidogen-2 (NID2) is a Key Factor in Collagen Causing Poor Response to Immunotherapy in Melanoma. Pharmacogenomics and Personalized Medicine, 16, 153-172.
Publication 2023
COL1A2 protein, human COL4A2 protein, human Col8A1 protein, human COL17A1 protein, human Collagen Genome, Human Melanoma Patients Phenotype
5
Genetic Analysis of hEDS Patients
The study group included 100 hEDS patients of Polish origin, women (84) and men (16), aged 17–63 years (median: 31 years). Patients were enrolled in the study by experienced clinical geneticists, according to the 2017 International Classification of the Ehlers-Danlos syndrome diagnostic criteria [1 (link)]. Joint hypermobility was evaluated on the Beighton scale. The control group consisted of 100 volunteers from the general Polish population matched by age and sex with the investigated group, who were healthy (including lack of EDS) at the time of the investigation and without a history of EDS in the family.
All hEDS patients or their parents provided informed consent to participate in the study. Consent to publish clinical/genetic data was also obtained from the patients or their parents.
The study was approved by the Ethics Committee of Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland (KB485/2013).
The analysis was performed on genomic DNA (gDNA), which was extracted from leukocytes (fibroblasts were not available) by QIAamp DNA Mini Kit (Qiagen, Germany) using standard procedures. In all patients, other types of EDS or other connective tissue disorders were excluded by testing them with NGS technology (Illumina NextSeq 550). The connective tissue disorder customer panel included COL5A1, COL5A2, COL3A1, COL1A1, COL1A2, TNXB, ADAMTS2, PLOD1, FKBP14, ZNF469, PRDM5, B4GALT7, B3GALT6, SLC39A13, CHST14, DSE, COL12A1, C1R, C1S, SEC23A, SEC24D, COL6A1, COL6A2, COL6A3, COL9A1, COL9A2, FBN1, FBN2, FLNA, and FLNB. Copy number variant (CNV) analysis was also performed. Sequencing data were aligned to the hg19 human reference genome. Based on the guidelines of the American College of Medical Genetics and Genomics, a minimum depth coverage of 30X was considered suitable for analysis. All patients negative for the NGS test were analysed for alterations in the SERPINH1 gene. Molecular analysis of the SERPINH1 gene was performed by Sanger sequencing (ABI3130XL) according to standard procedure (primer sequences available upon request). The pathogenicity of detected variants was assessed according to the ACMG guideline by Varsome [19 (link), 20 (link)].
Junkiert-Czarnecka A., Pilarska-Deltow M., Bąk A., Heise M, & Haus O. (2023). The role of gene encoding collagen secretion protein (SERPINH1) in the pathogenesis of a hypermobile type of Ehlers-Danlos syndrome. Advances in Dermatology and Allergology/Postȩpy Dermatologii i Alergologii, 40(1), 102-106.
Publication 2023
COL1A2 protein, human Connective Tissue Diseases Diagnosis Ehlers-Danlos Syndrome Ethics Committees Fibrillin-1 Fibroblasts Genes Genome Genome, Human Leukocytes Oligonucleotide Primers Parent Pathogenicity Patients PRDM5 protein, human Voluntary Workers Woman

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More about "COL1A2 protein, human"

The COL1A2 gene is responsible for producing one of the main components of type I collagen, the most abundant protein in the human body.
This structural protein is a crucial element of skin, bone, teeth, and connective tissues.
Mutations in the COL1A2 gene can lead to genetic disorders that affect collagen, such as osteogenesis imperfecta and Ehlers-Danlos syndrome.
Understanding the role of COL1A2 and its related pathways is essential for researching and developing treatments for these conditions.
Researchers can leverage cutting-edge protocols and AI-driven comparisons to optimize their COL1A2 protein research using platforms like PubCompare.ai.
To study COL1A2 expression, researchers may utilize techniques like TRIzol reagent or the RNeasy Mini Kit for RNA extraction, followed by a High-Capacity cDNA Reverse Transcription Kit for cDNA synthesis.
TaqMan Gene Expression Assays and the StepOnePlus Real-Time PCR System can then be used to quantify COL1A2 mRNA levels.
The IScript cDNA synthesis kit is another option for converting RNA to cDNA.
Additionally, compounds like Tamoxifen may be investigated for their effects on COL1A2 and related collagen pathways.
The TRI Reagent and RNeasy kit can also be employed for RNA isolation and purification in COL1A2-focused studies.
By leveraging these tools and techniques, researchers can deepen their understanding of the COL1A2 gene, its expression, and its involvement in collagen-related disorders, ultimately paving the way for more effective treatments and therapies.