CN116814804A - SNP (Single nucleotide polymorphism) marker related to erythrocyte RhD variant blood type - Google Patents
SNP (Single nucleotide polymorphism) marker related to erythrocyte RhD variant blood type Download PDFInfo
- Publication number
- CN116814804A CN116814804A CN202310703555.1A CN202310703555A CN116814804A CN 116814804 A CN116814804 A CN 116814804A CN 202310703555 A CN202310703555 A CN 202310703555A CN 116814804 A CN116814804 A CN 116814804A
- Authority
- CN
- China
- Prior art keywords
- rhd
- blood
- snp
- gene
- detecting
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Pending
Links
- 210000004369 blood Anatomy 0.000 title claims abstract description 51
- 239000008280 blood Substances 0.000 title claims abstract description 51
- 239000003550 marker Substances 0.000 title claims abstract description 17
- 210000003743 erythrocyte Anatomy 0.000 title claims description 11
- 239000002773 nucleotide Substances 0.000 title description 7
- 125000003729 nucleotide group Chemical group 0.000 title description 7
- 101150108975 Rhd gene Proteins 0.000 claims abstract description 63
- 108091026890 Coding region Proteins 0.000 claims abstract description 4
- 108091081024 Start codon Proteins 0.000 claims abstract description 4
- 108020004414 DNA Proteins 0.000 claims description 18
- 238000012163 sequencing technique Methods 0.000 claims description 17
- 238000012408 PCR amplification Methods 0.000 claims description 10
- 239000003153 chemical reaction reagent Substances 0.000 claims description 6
- 238000000034 method Methods 0.000 claims description 6
- 238000004458 analytical method Methods 0.000 claims description 3
- 108090000623 proteins and genes Proteins 0.000 abstract description 17
- 238000001514 detection method Methods 0.000 abstract description 9
- 238000012216 screening Methods 0.000 abstract description 5
- 150000001413 amino acids Chemical class 0.000 abstract description 3
- 230000000694 effects Effects 0.000 abstract description 2
- 102000004169 proteins and genes Human genes 0.000 abstract description 2
- 230000035772 mutation Effects 0.000 description 17
- HEDRZPFGACZZDS-UHFFFAOYSA-N Chloroform Chemical compound ClC(Cl)Cl HEDRZPFGACZZDS-UHFFFAOYSA-N 0.000 description 16
- 238000006243 chemical reaction Methods 0.000 description 14
- 239000006228 supernatant Substances 0.000 description 14
- LFQSCWFLJHTTHZ-UHFFFAOYSA-N Ethanol Chemical compound CCO LFQSCWFLJHTTHZ-UHFFFAOYSA-N 0.000 description 12
- PHTQWCKDNZKARW-UHFFFAOYSA-N isoamylol Chemical compound CC(C)CCO PHTQWCKDNZKARW-UHFFFAOYSA-N 0.000 description 8
- 239000000047 product Substances 0.000 description 8
- 239000000427 antigen Substances 0.000 description 7
- 102000036639 antigens Human genes 0.000 description 7
- 108091007433 antigens Proteins 0.000 description 7
- ISWSIDIOOBJBQZ-UHFFFAOYSA-N Phenol Chemical compound OC1=CC=CC=C1 ISWSIDIOOBJBQZ-UHFFFAOYSA-N 0.000 description 6
- KCXVZYZYPLLWCC-UHFFFAOYSA-N EDTA Chemical compound OC(=O)CN(CC(O)=O)CCN(CC(O)=O)CC(O)=O KCXVZYZYPLLWCC-UHFFFAOYSA-N 0.000 description 4
- 230000003321 amplification Effects 0.000 description 4
- 230000009286 beneficial effect Effects 0.000 description 4
- 238000012217 deletion Methods 0.000 description 4
- 230000037430 deletion Effects 0.000 description 4
- 238000003745 diagnosis Methods 0.000 description 4
- 230000001788 irregular Effects 0.000 description 4
- 239000000203 mixture Substances 0.000 description 4
- 238000003199 nucleic acid amplification method Methods 0.000 description 4
- 210000005259 peripheral blood Anatomy 0.000 description 4
- 239000011886 peripheral blood Substances 0.000 description 4
- 150000002989 phenols Chemical class 0.000 description 4
- 239000002244 precipitate Substances 0.000 description 4
- 201000010099 disease Diseases 0.000 description 3
- 208000037265 diseases, disorders, signs and symptoms Diseases 0.000 description 3
- 239000002243 precursor Substances 0.000 description 3
- 230000000405 serological effect Effects 0.000 description 3
- 108010067770 Endopeptidase K Proteins 0.000 description 2
- 241000282414 Homo sapiens Species 0.000 description 2
- 241000282560 Macaca mulatta Species 0.000 description 2
- VMHLLURERBWHNL-UHFFFAOYSA-M Sodium acetate Chemical compound [Na+].CC([O-])=O VMHLLURERBWHNL-UHFFFAOYSA-M 0.000 description 2
- 239000007983 Tris buffer Substances 0.000 description 2
- -1 Tris saturated phenol Chemical class 0.000 description 2
- 238000000246 agarose gel electrophoresis Methods 0.000 description 2
- 239000003146 anticoagulant agent Substances 0.000 description 2
- 229940127219 anticoagulant drug Drugs 0.000 description 2
- 230000010100 anticoagulation Effects 0.000 description 2
- 238000005119 centrifugation Methods 0.000 description 2
- 239000003086 colorant Substances 0.000 description 2
- 238000002474 experimental method Methods 0.000 description 2
- 238000000605 extraction Methods 0.000 description 2
- 239000012634 fragment Substances 0.000 description 2
- 230000008014 freezing Effects 0.000 description 2
- 238000007710 freezing Methods 0.000 description 2
- 230000002949 hemolytic effect Effects 0.000 description 2
- 230000002757 inflammatory effect Effects 0.000 description 2
- 238000004519 manufacturing process Methods 0.000 description 2
- 239000008188 pellet Substances 0.000 description 2
- 230000002093 peripheral effect Effects 0.000 description 2
- 238000005070 sampling Methods 0.000 description 2
- 238000007480 sanger sequencing Methods 0.000 description 2
- 235000017281 sodium acetate Nutrition 0.000 description 2
- 239000001632 sodium acetate Substances 0.000 description 2
- 238000010257 thawing Methods 0.000 description 2
- 238000011282 treatment Methods 0.000 description 2
- XLYOFNOQVPJJNP-UHFFFAOYSA-N water Substances O XLYOFNOQVPJJNP-UHFFFAOYSA-N 0.000 description 2
- 108020004705 Codon Proteins 0.000 description 1
- 206010018910 Haemolysis Diseases 0.000 description 1
- 206010067122 Haemolytic transfusion reaction Diseases 0.000 description 1
- 108091028043 Nucleic acid sequence Proteins 0.000 description 1
- 208000025174 PANDAS Diseases 0.000 description 1
- 208000021155 Paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection Diseases 0.000 description 1
- 240000000220 Panda oleosa Species 0.000 description 1
- 235000016496 Panda oleosa Nutrition 0.000 description 1
- 208000003441 Transfusion reaction Diseases 0.000 description 1
- 238000010521 absorption reaction Methods 0.000 description 1
- 210000000349 chromosome Anatomy 0.000 description 1
- 230000007547 defect Effects 0.000 description 1
- 238000010586 diagram Methods 0.000 description 1
- 238000009792 diffusion process Methods 0.000 description 1
- 230000002068 genetic effect Effects 0.000 description 1
- ZDXPYRJPNDTMRX-UHFFFAOYSA-N glutamine Natural products OC(=O)C(N)CCC(N)=O ZDXPYRJPNDTMRX-UHFFFAOYSA-N 0.000 description 1
- 230000008588 hemolysis Effects 0.000 description 1
- HNDVDQJCIGZPNO-UHFFFAOYSA-N histidine Natural products OC(=O)C(N)CC1=CN=CN1 HNDVDQJCIGZPNO-UHFFFAOYSA-N 0.000 description 1
- 230000002163 immunogen Effects 0.000 description 1
- 238000001802 infusion Methods 0.000 description 1
- 238000003780 insertion Methods 0.000 description 1
- 230000037431 insertion Effects 0.000 description 1
- 108020004999 messenger RNA Proteins 0.000 description 1
- 238000012544 monitoring process Methods 0.000 description 1
- 102000054765 polymorphisms of proteins Human genes 0.000 description 1
- 230000035935 pregnancy Effects 0.000 description 1
- 238000012360 testing method Methods 0.000 description 1
- 230000007704 transition Effects 0.000 description 1
- 238000012795 verification Methods 0.000 description 1
Abstract
The invention aims to provide an SNP marker for detecting a RhD gene polymorphism site, wherein the SNP marker is that the coding region of the RhD gene is mutated from a start codon to a 414 th base and from G to T; resulting in a change in amino acid 138 and thus in a conformational change in the protein. The SNP locus obtained by detection and screening is provided, so that an effective path for diagnosing the gene of the RhD blood group is provided, and the application effect shows that the SNP locus and the detection primer of the gene provided by the invention can be effectively used for rapidly detecting the gene of the RhD of clinical patients and blood station blood donors.
Description
Technical Field
The invention belongs to the technical field of gene diagnosis products, and particularly relates to an SNP marker related to erythrocyte RhD variation blood types.
Background
The Rh blood group system (Rhesus monkeys) was first discovered by a well-known scientist, nobel prize Karl Landsteiner from red blood cells of Rhesus monkeys, and is therefore named. The Rh blood group system is the most complex of 36 blood group systems of human beings at present, and the importance of the Rh blood group system is inferior to that of the ABO system, so that the Rh blood group system plays an important role in clinical blood transfusion and diagnosis and treatment of neonatal hemolytic diseases. The D antigen in Rh blood group system is the most immunogenic and polymorphic. For Han people, the RhD negative population is about three thousandths, and is also called panda blood because of very rare people.
Because of the strong antigenicity of RhD, a RhD-negative person cannot receive RhD-positive blood because the RhD antigen will stimulate the production of anti-RhD antibodies in a RhD-negative human. If RhD positive blood is re-infused, a hemolytic transfusion reaction may result. Also, if RhD negative women stimulate anti-RhD antibodies in the body due to pregnancy or blood transfusion, re-pregnancy may lead to the occurrence of hemolysis of the newborn.
In addition to the normal RhD positive and negative, the RhD blood group system has many variants including weak D (weak D), partial D (partial D), and DEL (diffuse). The presence of incomplete or mutated RhD antigens on the surface of these mutated erythrocytes may also stimulate the production of antibodies if infused into negative individuals, and thus these mutated individuals have two main characteristics: firstly, they are two different treatments as recipients and donors, as recipients, they can only input RhD negative blood; while as donors, their blood can only be used as RhD positive blood. Secondly, the detection is easy to miss. Because of the variation of RhD antigen, frequent antibodies cannot react with the RhD antigen in the conventional blood group serological detection, the RhD antigen is easily judged to be RhD negative, and no particularly effective measure for eliminating irregular antibodies exists at present, so the RhD antigen is extremely harmful to patients needing multiple blood transfusion and pregnant women. The accurate typing is a precondition for ensuring correct infusion, and the conventional blood type detection method is a serological experiment, but the experiment is limited by various limitations, such as the quality of a sample, the interference of autoantibodies or irregular antibodies, the influence of diseases and the like, and the class which can only be detected by an absorption and diffusion test is not judged for the DEL type, so that the diagnosis is required to be carried out at the gene level by utilizing a molecular biology method.
Disclosure of Invention
The invention aims to provide an SNP marker related to erythrocyte RhD variant blood types, and the erythrocyte RhD variant blood types can be screened by detecting the SNP marker, so that the defects of the prior art are overcome.
The invention firstly provides a SNP marker related to the variation blood type of RhD, which is characterized in that the 414 th base of the coding region of the RHD gene is mutated from a start codon to T by G mutation.
The invention also provides an application of the SNP marker in preparing a product for detecting the red blood cell RhD variant blood type;
the product is a PCR amplification sequencing reagent;
the invention also provides a PCR amplification sequencing reagent for detecting the RhD variant blood type, which comprises a primer pair for detecting the SNP marker;
the sequence information of the primer pair and the primer is as follows:
RHD-3F:5′-CCACAGAAAGTAGGTGCCCAA-3′(SEQ ID NO:1)
RHD-3R:5′-TCTTTATTTTTCAAAACCCTGGAAA-3′(SEQ ID NO:2)。
the invention also provides a method for detecting the erythrocyte RhD variant blood type, which comprises the steps of carrying out PCR amplification on the DNA of the blood sample to be detected through the primer capable of amplifying the SNP marker, sequencing the amplified product, and carrying out genotype analysis to determine whether the SNP marker exists in the sample to be detected.
The SNP locus obtained by detection and screening is provided, so that an effective way for carrying out RhD blood group gene diagnosis is provided, and the application effect shows that the SNP locus and the detection primer provided by the invention can be effectively used for carrying out quick detection on RHD genes of clinical patients and blood station blood donors.
Drawings
Fig. 1: rhD variant phenotype RhD gene sequencing diagram of example 1, wherein a: male parent of the first person, normal RhD positive phenotype, carrying RhD total deletion gene; b: mother with first evidence, normal RhD positive phenotype, carrying mutant gene; in the family, the coding regions of two RHD genes are mutated from the 414 th base of the start codon and from G to T.
Detailed Description
The applicant carried out RhD gene sequencing from 626 serological individuals who were negative for RhD or variant, and found that a new SNP mutation resulted in RhD variant, thereby leading to the present invention.
The RH gene is located in the region of chromosome 1p34.3-1p36.1, and can be transcribed into 2837bp mRNA (NCBI accession No. NM-016124.4) and finally translated into 417 amino acid protein. The RHD gene detection system is established by adopting a molecular biological means, is applied to clinical and blood collection work, is beneficial to accurately detecting RhD negative individuals, is beneficial to reducing the generation of irregular antibodies of blood recipients, is beneficial to preventing and monitoring prenatal irregular antibodies, and is beneficial to reducing the occurrence of hemolytic diseases of newborns.
For the terms involved in the present invention, the applicant interprets as follows:
SNP (single nucleotide polymorphism, SNP, a single nucleotide polymorphism) refers to a polymorphism in a DNA sequence at the genomic level caused by a variation of a single nucleotide. SNPs exhibit polymorphisms that involve only single base variation, in terms of transitions, transversions, insertions, deletions, and the like.
The present invention will be described in detail with reference to examples.
Example 1: screening of SNP markers
1. Extracting peripheral blood genome DNA:
2-5mL of peripheral venous blood of RhD negative or variant blood donors is extracted on the basis of agreement of sampling objects and in accordance with national relevant policy regulations, and is put into an EDTA anticoagulation tube for freezing storage at-80 ℃ for standby; after thawing frozen EDTA anticoagulants at room temperature, 500. Mu.L was placed in a centrifuge tube, added with an equal volume of TE (pH 8.0), mixed well, centrifuged at 4℃for 10 minutes at 10000rpm, and the supernatant was discarded.
180. Mu.L TE, 20. Mu.L LSDS (10%), 8. Mu.L proteinase K (L0 mg/ml) were added and mixed well and placed in a 37℃water bath overnight. The sample was removed from the water bath and the pellet was centrifuged instantaneously. An equal volume of Tris-saturated phenol (about 300. Mu.L) was added to the reaction tube, thoroughly mixed, centrifuged at 10000rpm for 10 minutes at room temperature, and the supernatant (about 300. Mu.L) was pipetted into a new centrifuge tube. Phenol extraction was repeated once and the supernatant was aspirated into a new centrifuge tube.
Equal volumes of Tris-saturated phenol/chloroform mixture (150. Mu.L of phenol/chloroform each) were added, mixed well, centrifuged at 10000rpm for 10 minutes at room temperature and the supernatant was transferred to a new centrifuge tube.
Equal volumes of Tris saturated phenol, chloroform: isoamyl alcohol mixture (100. Mu.L each of phenol, chloroform, isoamyl alcohol) were added, mixed well, centrifuged at 10000rpm for 10 minutes at room temperature, and the supernatant was transferred to a new centrifuge tube.
1/10 volumes of 3mol/L sodium acetate (about 30. Mu.L) pH5.2 was added, 2 volumes of pre-chilled 100% ethanol, gently mixed, and a white flocculent precipitate was seen. The DNA was precipitated at the bottom of the tube by centrifugation at 10000rpm for 10 minutes at room temperature, and the supernatant was discarded.
70% ethanol was added to the DNA precipitate, rinsed once, centrifuged at 7000rpm at room temperature for 5 minutes, the supernatant was discarded, the remaining ethanol was evaporated at room temperature, and finally 50. Mu.L TE (pH 8.0) was added thereto, and the DNA was dissolved overnight at 4 ℃.
And (3) performing agarose gel electrophoresis on the extracted DNA, and detecting the purity and concentration of the DNA by using an ultraviolet spectrophotometer to compare colors at 260nm and 280 nm.
2. Direct sequencing to find mutations in the donor RHD gene
PCR amplification of the fragment of interest: reaction conditions and reaction system:
(1) PCR reaction conditions: 5m at 95 ℃;95℃30s,58℃30s,72℃60s,35cycles; 5m at 72 ℃.
(2) The reaction system: (Onlambda company Fast startTaq polymerase)
The reaction system is used for respectively carrying out the amplification reaction of the genome DNA template of each RhD negative or D variant blood donor and the RhD primer.
Sequencing PCR products: the PCR products were sequenced using conventional Sanger sequencing, RHD-3F:5'-CCACAGAAAGTAGGTGCCCAA-3', a mutation was found at the third exon of the RHD gene of the rhD mutant donor, base G at position 414 was mutated to T (FIG. 1), resulting in mutation of nt412-414 from CAG to CAT, amino acid codon from glutamine (Gln) to histidine (His), resulting in conformational changes in the RhD protein, and serology showed a RhD mutant phenotype. Multiple sequencing results indicate that the mutation site is not introduced by amplification or sequencing errors and should be a new mutation.
This mutation was not present in the following four databases: single nucleotide polymorphism databases (ftp:// ftp. Ncbi. Gov/snp/database /), thousand person genome project (ftp:// ftp-trace. Ncbi. Gov/1000 genome/ftp /), hapmap8 databases (http:// Hapmap. Ncbi. Nlm. Gov /), and inflammatory Huang Shuju libraries (http:// yh. Genemics. Org. Cn /). This mutation results in a conformational change in the RhD protein, resulting in a RhD variant. In contrast, mutation screening at this site was performed on a sample of peripheral blood genomic DNA from 200 RhD-positive blood donors, and no mutation was found.
Through the analysis, the method can accurately determine the RHD gene, thereby more accurately determining the RHD blood type of the person to be tested, and having important significance for the patient to make transfusion policies.
Example 2: genetic verification of parents of SNP mutant precursor
1. Extracting peripheral blood genome DNA:
2-5mL of peripheral venous blood of RhD negative or variant blood donors is extracted on the basis of agreement of sampling objects and in accordance with national relevant policy regulations, and is put into an EDTA anticoagulation tube for freezing storage at-80 ℃ for standby; after thawing frozen EDTA anticoagulants at room temperature, 500. Mu.L was placed in a centrifuge tube, added with an equal volume of TE (pH 8.0), mixed well, centrifuged at 4℃for 10 minutes at 10000rpm, and the supernatant was discarded.
180. Mu.L TE, 20. Mu.L LSDS (10%), 8. Mu.L proteinase K (L0 mg/ml) were added and mixed well and placed in a 37℃water bath overnight. The sample was removed from the water bath and the pellet was centrifuged instantaneously. An equal volume of Tris-saturated phenol (about 300. Mu.L) was added to the reaction tube, thoroughly mixed, centrifuged at 10000rpm for 10 minutes at room temperature, and the supernatant (about 300. Mu.L) was pipetted into a new centrifuge tube. Phenol extraction was repeated once and the supernatant was aspirated into a new centrifuge tube.
Equal volumes of Tris-saturated phenol/chloroform mixture (150. Mu.L of phenol/chloroform each) were added, mixed well, centrifuged at 10000rpm for 10 minutes at room temperature and the supernatant was transferred to a new centrifuge tube.
Equal volumes of Tris saturated phenol, chloroform: isoamyl alcohol mixture (100. Mu.L each of phenol, chloroform, isoamyl alcohol) were added, mixed well, centrifuged at 10000rpm for 10 minutes at room temperature, and the supernatant was transferred to a new centrifuge tube.
1/10 volumes of 3mol/L sodium acetate (about 30. Mu.L) pH5.2 was added, 2 volumes of pre-chilled 100% ethanol, gently mixed, and a white flocculent precipitate was seen. The DNA was precipitated at the bottom of the tube by centrifugation at 10000rpm for 10 minutes at room temperature, and the supernatant was discarded.
70% ethanol was added to the DNA precipitate, rinsed once, centrifuged at 7000rpm at room temperature for 5 minutes, the supernatant was discarded, the remaining ethanol was evaporated at room temperature, and finally 50. Mu.L TE (pH 8.0) was added thereto, and the DNA was dissolved overnight at 4 ℃.
And (3) performing agarose gel electrophoresis on the extracted DNA, and detecting the purity and concentration of the DNA by using an ultraviolet spectrophotometer to compare colors at 260nm and 280 nm.
2. Direct sequencing to find mutation of the second exon of the parent RHD gene of the precursor
PCR amplification of the fragment of interest: reaction conditions and reaction system:
(1) PCR reaction conditions: 5m at 95 ℃;95℃30s,58℃30s,72℃60s,35cycles; 5m at 72 ℃.
(2) The reaction system: (Onlambda company Fast startTaqpolymerase)
The reaction system is used for respectively carrying out the amplification reaction of the genome DNA template and the amplification primer of the parent of the forerunner.
Sequencing PCR products: sequencing the PCR product by adopting a conventional Sanger sequencing method (figure 1), wherein the male parent (A) of the forensic person is of a normal RhD positive phenotype, and carrying the RHD total deletion gene; the mother (B) of the forerunner is of a normal RhD positive phenotype, carries mutant genes and shows heterozygous peaks of the RHD normal genes and SNP mutant genes; the result shows that the precursor (C) inherits the complete deletion gene of the father RHD and the SNP mutant gene of the mother, so the variant phenotype of the RHD is shown.
This mutation was not present in the following four databases: single nucleotide polymorphism databases (ftp:// ftp. Ncbi. Gov/snp/database /), thousand genome project (ftp:// ftp-trace. Ncbi. Gov/1000 genome/ftp /), hapmap8 database (http:// Hapmap. Ncbi. Nlm. Gov /), and inflammatory Huang Shuju library (http:// yh. Genetics. Org. Cn /), indicate that the mutation is very rare. In contrast, mutation screening at this site was performed on a sample of peripheral blood genomic DNA from 200 RhD-positive blood donors, and no mutation was found.
The experimental result shows that the SNP mutation site can accurately determine the RhD blood type of a person to be tested, and has important significance for making a blood transfusion policy for patients.
Claims (7)
1. A SNP marker related to the variation blood type of RhD, characterized in that the SNP marker is positioned at the 414 th base from the start codon in the coding region of the RHD gene, and is G or T.
2. The use of the SNP marker of claim 1 for preparing a preparation for detecting erythrocyte RhD variant blood type.
3. The use of claim 2, wherein the preparation is a PCR amplification sequencing reagent.
4. A PCR amplification sequencing reagent for detecting RhD variant blood types, wherein the PCR amplification sequencing reagent comprises a primer pair for detecting the SNP markers of claim 1.
5. The PCR amplification sequencing reagent of claim 4, wherein the primer pair has the sequences SEQ ID NO. 1 and SEQ ID NO. 2.
6. A method for detecting the variation blood type of red blood cell RhD is characterized in that the PCR amplification is carried out on the DNA of a blood sample to be detected through a primer capable of amplifying the SNP marker according to claim 1, and the genotype analysis is carried out after the sequencing of the amplified product, so that whether the SNP marker exists in the sample to be detected is determined.
7. The method of claim 6, wherein the primer pair has the sequences SEQ ID NO. 1 and SEQ ID NO. 2.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202310703555.1A CN116814804A (en) | 2023-06-14 | 2023-06-14 | SNP (Single nucleotide polymorphism) marker related to erythrocyte RhD variant blood type |
Applications Claiming Priority (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202310703555.1A CN116814804A (en) | 2023-06-14 | 2023-06-14 | SNP (Single nucleotide polymorphism) marker related to erythrocyte RhD variant blood type |
Publications (1)
| Publication Number | Publication Date |
|---|---|
| CN116814804A true CN116814804A (en) | 2023-09-29 |
Family
ID=88128583
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CN202310703555.1A Pending CN116814804A (en) | 2023-06-14 | 2023-06-14 | SNP (Single nucleotide polymorphism) marker related to erythrocyte RhD variant blood type |
Country Status (1)
| Country | Link |
|---|---|
| CN (1) | CN116814804A (en) |
-
2023
- 2023-06-14 CN CN202310703555.1A patent/CN116814804A/en active Pending
Similar Documents
| Publication | Publication Date | Title |
|---|---|---|
| CN106834287B (en) | SNP marker for detecting RhD negative phenotype | |
| Orzińska et al. | Prediction of fetal blood group and platelet antigens from maternal plasma using next‐generation sequencing | |
| JP2022024127A (en) | Detecting hematological disorders using cell-free dna in blood | |
| CN105506107A (en) | Primers and method for detecting polymorphic hotspot mutation condition of DOCK2 gene | |
| CN106636420B (en) | SNP site of ABO blood type variant for triggering hemolytic transfusion reaction | |
| CN109735610B (en) | Gene polymorphism site for detecting Bombay-like blood type | |
| CN106967808B (en) | Primer group for detecting RhD negative blood type and application thereof | |
| CN108998525A (en) | Detect primer, method and the kit of ATRX gene point mutation | |
| CN107190071B (en) | It is a kind of for detecting the SNP marker of RhD variation phenotypes | |
| CN111808937A (en) | Fut 1508 dupT allele of Bombay blood group and detection method and application thereof | |
| CN111304311A (en) | SNP marker for detecting O gene mutation in ABO blood group system | |
| CN116814804A (en) | SNP (Single nucleotide polymorphism) marker related to erythrocyte RhD variant blood type | |
| CN109486946A (en) | It is a kind of for detecting the SNP site of RHD blood group anomaly | |
| CN109321638A (en) | Detect primer, method and the kit of the 15th exon site mutation of TSC1 | |
| CN114317550A (en) | Nucleic acid for coding MITF gene mutant and application thereof | |
| CN107058531A (en) | A kind of kit and method for detecting Niemann-Pick disease SMPD1 gene mutations | |
| CN117286241A (en) | SNP marker for detecting RhD negative phenotype easy to miss | |
| CN114561458B (en) | SNP locus related to B variant in ABO blood group system and application thereof | |
| CN117887836A (en) | SNP marker for detecting weak expression RhD variant | |
| CN113481289B (en) | Primer composition for detecting sideroblastic red blood cell anemia and application thereof | |
| CN112760370B (en) | SNP site of MNS blood group system N antigen for initiating hemolytic blood transfusion reaction | |
| CN114381513B (en) | Biomarker related to X-linked lymphoproliferative disorder and application thereof | |
| CN117757798A (en) | Hereditary microcephaly pathogenic mutant gene and application thereof | |
| EP1990426A1 (en) | A method for preparing the primers for in vitro identifying mutations within larged vestibular aqueduct syndromic hearing loss pds gene and the use thereof | |
| He et al. | Identification and analysis of a rare CisAB group |
Legal Events
| Date | Code | Title | Description |
|---|---|---|---|
| PB01 | Publication | ||
| PB01 | Publication | ||
| SE01 | Entry into force of request for substantive examination | ||
| SE01 | Entry into force of request for substantive examination |