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Can rh negative blood be cloned?

It has been observed that without RH protein, the cloned blood cell loses its required flexibility as well as the DNA strand is difficult to use after retrieving it. The root cause for this is related to the D antigen, its genetic makeup and receptors variations. In combination, all these factors make it difficult to clone RH negative blood cells and thus also in whole.

OK so in practice this means what: It is harder to clone, but it can and/or is being done?

It has been estimated that 85 % of all humans’ beings are with RH Positive blood type.

For the world the number is around 7%.
I am looking for information regarding the rh negative blood factor.
Dear rhnegnet,

Yes as mentioned,

It has been estimated that 85 % of all humans’ beings are with RH Positive blood type
It is 85% in Europe. In the world it is around 93%.

Rh negative population in Europe: 15%.
Worldwide: 7%


OK so in practice this means what: It is harder to clone, but it can and/or is being done?

I am looking for information regarding the rh negative blood factor.
There are over 30 human blood group systems, out of which two are the major ones- ABO system and Rh system. A blood group system basically refers to a group of proteins (antigens) whose presence or absence on an erythrocyte (red blood cell) is used in classification of a person’s blood type. For e.g. If you have A antigen on your red blood cells, your blood type is A; if you have B antigen on your RBCs your blood type is B. If a person has both A and B antigens then his/her blood type is AB and absence of both means O blood type.

The Rh blood group system is used in addition to the ABO system as a suffix i.e. presence of Rh factor in an individual of A/B/AB/O blood type means that individual is A+/B+/AB+/O+. Absence of the Rh factor is denoted by A-/B-/AB-/O-.

The ‘Rh factor’ was first discovered around 1939 when Drs. Levine and Stenton first talked about hemolytic blood transfusion and hemolytic disease of the newborn. These terms refer to the agglutination reaction that occurs between Rh+ and Rh- blood types. Since the Rh factor had still not been recognized by then, the doctors conducted experiments and the results showed that the blood sample ( Rh-) showed agglutination reaction with more than 80% of the blood samples present. This study along with Landsteiner and Weiner’s in 1940 on rabbits immunized with RBCs of Rhesus monkeys was able to corroborate presence of a factor that was responsible for the agglutination reaction. Landsteiner and Weiner named this factor as Rhesus factor because of the se of RBCs of Rhesus monkeys.

Further studies on human blood cells and immunized rabbit blood cells revealed that the antigens found on human RBCs are serologically similar to the Rh factor in monkeys, but not identical. However, by then the name had stuck. Hence the term Rh factor was used to denote antigens while anti-Rh referred to antibodies against those antigens.

Naming of the Rh protein and genes associated with it proved to be more complicated. There are two nomenclature procedures that are most widely followed. The Fischer-Race nomenclature is on the basis of the hypothesis that 3 genes produce proteins for the blood group system and multiple proteins are involved in the CDE system where presence of D antigen gives Rh+ blood and absence of it ( d state) gives Rh- blood. Another system is the Weiner system which is based on the hypothesis that there is one gene producing multiple proteins. However, on analysis it was found that neither of these hypotheses is fully correct. Results of the study indicated that two genes are involved- a single gene-single protein system and a single gene- multiple protein system.

The structural difference between an Rh positive and an Rh negative individual is polymorphism of gene responsible for D antigen. As it was established, 2 genes are responsible for the Rh blood group system- one gene codes for D antigen and another codes for C, c, E, e proteins. The latter gene is present in all individuals irrespective of their phenotype. T

The phenotypic differences arise due to polymorphism of the first gene or the RhD gene. The RhD gene is present in Rh + individuals and lacking in Rh- individuals. Mouro et al’s paper on the structure of the RhD polypeptide showed that the RhD mRNA gives rise to 417 AA polypeptide ( D antigen) with a molecular weight around 45500 Da. The Cc/Ee polypeptide is similar to the D polypeptide with variations in only 36 amino acids.

Scientists have successfully cloned the RhD gene and on studying the expression product it was found that the mRNA gave rise to RhD and RhCcEe proteins. The mRNA produced showed no relation to RhD negative individuals. Further attempts at cloning the RhD negative gene showed that though the RhCcEe gene can be cloned, it is unstable without the RhD gene and doesn’t survive. Due to the lack of success in cloning experiments and the need for RhD- blood, scientists have developed RhD- blood derived from animals and have even developed methods to convert Rh+ to Rh-.

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Can rh negative blood be cloned?00