We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Yehudit Bergman is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2000 — 2003 |
Bergman, Yehudit |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular Mechanisms Underlying Lgk Allelic Exclusion @ Hebrew University of Jerusalem
DESCRIPTION (adapted from investigator's abstract): One of the most interesting phenomena associated with gene rearrangement in the immune system is allelic exclusion, in which individual B- and T-cells express one specific antigen-receptor molecule. In order to guarantee the production of a unique receptor-type per cell, the immune system includes mechanisms for restricting expression to only one out of the two possible alleles. The investigator's recent experiments indicate that in B-cells that contain one unmethylated rearranged gene, the germline allele is methylated, proving that the initial demethylation is monoallelic, and strongly suggesting that it is this modification that marks the allele for rearrangement and expression. However, it is not yet clear how one allele is marked for demethylation. In order to understand this process the investigator will identify the cis-acting elements and the trans-acting factors that are involved in demethylation of a single allele. The possibility that one allele is more accessible than the other will be investigated, and the role of chromatin structure and germline transcription in this process will be studied. A likely possibility is that the two alleles are actually marked during the initial stages of B-cell development or even earlier. This results in both chromosomes having a different local structure. In keeping with this idea, the kappa genes have been found to be located within an asynchronously replicating chromosomal domain. Thus, it is proposed to decipher the molecular mechanisms that underlie the process of asynchronous replication. With this information in hand, the investigator will study the possible link between replication, chromatin accessibility and methylation, and their role in kappa chain rearrangement during normal B-cell development and in allelic exclusion. This may be very similar to what happens in the process of X-chromosome inactivation, where asynchronous replication and methylation differentially mark the two chromosomes.
|
1 |
2006 — 2009 |
Bergman, Yehudit |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Epigenetic Mechanisms Controlling Igk Allelic Exclusion @ Hebrew University of Jerusalem
[unreadable] DESCRIPTION (provided by applicant): Monoallelic gene expression, or allelic exclusion, is critical to the functioning of the immune system as it allows each lymphocyte to elaborate an antigen receptor of a single type. Chaos in immune system regulation might ensue if, for example, a B cell expressed both an antibody that responded to a pathogen and a second antibody that would cause damage to a certain host system. It has been proposed that the major pathway for implementing this choice is by a feedback mechanism in which the generation of a gene product from one allele leads to inhibition of the recombination machinery, thereby preventing rearrangement on the remaining germ line allele. While this mechanism may certainly play a maintenance role in inhibiting rearrangement on the non-selected allele, recent evidence suggests that the process of allelic exclusion may actually begin early in development, at about the time of implantation, when the antigen receptor genes become asynchronously replicating in each cell. However, it is not yet known how this chromosomal mark enables the initial selection of only one allele. We have designed experiments using targeted transgenic mice to show that replication timing plays a critical and direct role in controlling allelic exclusion. We will identify the molecular components that set up the asynchronous pattern of replication. We have developed a unique clonal pre-B cell system that allows us to decipher the monoallelic epigenetic processes such as chromatin modifications, unequal nuclear localization, DMA methylation, and replication that leads to allelic exclusion. These epigenetic mechanisms may be very similar to those that regulate the X-chromosome inactivation in female cells and parental genomic imprinting. These studies will help us to understand how the diversity and specificity of the immune system are generated and how this system functions to eliminate pathogens. [unreadable] [unreadable]
|
1 |