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Is there loss of BRCA1 and increase in 53BP1 in progeria?

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Loss of BRCA1 and an increase in 53BP1 are observed in the context of age-associated DNA repair deficiencies. In aged human mammary epithelial cells, a decrease in the activity of homologous recombination (HR) pathways, including BRCA1, is reported, along with deficient recruitment of 53BP1 to DNA double-strand break sites, leading to a switch to alternative repair mechanisms. Additionally, the inactivation of 53BP1 in BRCA1 mutant cells reduces translesion synthesis (TLS)-specific mutagenesis, indicating a regulatory role of 53BP1 in DNA damage bypass pathways. However, there is no direct mention of the specific relationship between BRCA1 loss and 53BP1 increase in progeria in the provided contexts.

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Open access•Posted Content•DOI RAD52 underlies the synthetic-lethal relationship between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta loss Katarzyna Starowicz, George Ronson, Elizabeth Anthony, Lucy Clarke, Alexander J Garvin, Andrew D Beggs, Celina Whalley, Matthew Edmonds, James F.J. Beesley, Joanna R. Morris - Show less +9 more 20 Mar 2022-bioRxiv	Not addressed in the paper.
Open access•Journal Article•DOI Age-associated deficient recruitment of 53BP1 in G1 cells directs DNA double-strand break repair to BRCA1/CtIP-mediated DNA-end resection. Teresa Anglada, Anna Genescà, Marta Martín - Show less +2 more 27 Dec 2020 5 Citations	Not addressed in the paper.
Open access•Journal Article•DOI BRCA1 deficiency specific base substitution mutagenesis is dependent on translesion synthesis and regulated by 53BP1 Dan Chen, Judit Gervai, Ádám Póti, Eszter Nemeth, Zoltán Szeltner, Bernadett Szikriszt, Zsolt Gyüre, Judit Zámborszky, Marta Ceccon, F. D'Adda Di Fagagna, Zoltan Szallasi, Andrea L. Richardson, Dávid Szüts - Show less +12 more 11 Jan 2022-Nature Communications 10 Citations	Not addressed in the paper.
Posted Content•DOI Data from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors 03 Apr 2023	Not addressed in the paper.
Posted Content•DOI Data from Loss of 53BP1 Causes PARP Inhibitor Resistance in <i>Brca1</i>-Mutated Mouse Mammary Tumors 03 Apr 2023	Not addressed in the paper.

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Is RIng1b Downregulated in Progeria?5 answersYes, RIng1b is downregulated in progeria. Studies have shown that in Hutchinson-Gilford progeria syndrome (HGPS), the expression of RIng1b is decreased in comparison to normal cells. Additionally, research on Zmpste24-deficient mice, a model for progeria, revealed that impaired insulin-like growth factor 1 receptor (IGF-1R)/Akt signaling leads to premature aging, where progerin interacts with IGF-1R, downregulating its expression and causing cellular senescence. Furthermore, in HGPS, a longitudinal gene expression analysis demonstrated a progressive activation of Rho signaling and SerpinE1, with siRNA-mediated downregulation of SerpinE1 reversing key pathological features of HGPS, indicating its role in the disease. These findings collectively support the downregulation of RIng1b in progeria conditions.

What is the relationship between progeria and alterations in xrcc1 ?5 answersXRCC1 alterations have been linked to various cancers, including glioma, breast cancer, and colorectal cancer, but not specifically to progeria. In glioma, reduced XRCC1 expression was associated with cancer progression, indicating a potential tumor suppressor role. In breast cancer, XRCC1 gene polymorphisms were studied, highlighting its involvement in cancer development. Additionally, XRCC1 polymorphisms were associated with testicular germ cell tumors, affecting genomic instability and tumor progression. In colorectal cancer, XRCC1 alterations were not directly mentioned, but the study focused on chromosomal instability and microsatellite instability as important genetic alterations. However, no direct relationship between XRCC1 alterations and progeria was found in the provided contexts.

How is ku70 changed in progeria cells?5 answersIn progeria cells, Ku70 plays a significant role in DNA repair processes and cellular abnormalities. The presence of progerin, an abnormal lamin A protein, leads to disrupted nuclear architecture, chromatin organization, and gene expression in Hutchinson-Gilford progeria syndrome (HGPS) cells. Additionally, Ku70 is involved in repairing DNA double-strand breaks (DSBs) and is crucial for cellular response to DNA-damaging agents in prostate cancer cells. Moreover, Ku70 is part of the classical nonhomologous end joining (C-NHEJ) repair pathway, where its deficiency can impact the repair of DSBs and lead to cellular abnormalities in G1-phase progenitor B cells. Acetylation of specific lysine residues in the Ku70 nuclear localization signal (NLS) can regulate the subcellular localization of Ku, affecting its function in DNA repair processes.

Is ezh2 upregulated in progeria cells?4 answersEZH2 is not specifically mentioned in the contexts provided in relation to progeria cells. However, the data from the contexts highlights the role of EZH2 in various cancers, such as lung cancer, prostate cancer, and acute myeloid leukemia. EZH2 is implicated in cancer progression, metastasis, and immune infiltration modulation. It is regulated by proteins like USP44 and has prognostic value in different cancer types. While EZH2 is not directly linked to progeria cells in the provided contexts, its involvement in cancer development and progression suggests a potential avenue for exploration in the context of progeria. Further research would be needed to determine if EZH2 is upregulated in progeria cells.

How is xrcc1 regulated in progeria?5 answersXRCC1 regulation in progeria involves various mechanisms. Studies show that XRCC1 plays a crucial role in DNA repair processes. In the context of progeria, dysregulation of XRCC1 can impact DNA repair efficiency, contributing to accelerated aging phenotypes. Specifically, XRCC1 expression can be influenced by factors like PARP1 activity, STAT3 signaling, and epigenetic modifications mediated by KDM5B. These regulatory pathways affect XRCC1 levels and function, potentially leading to impaired DNA repair in progeria. Understanding the intricate regulation of XRCC1 in the context of progeria sheds light on potential therapeutic targets to mitigate the effects of accelerated aging associated with this condition.

Is progerin seen to accumulate in normal aging cells?5 answersProgerin, a truncated form of lamin A, is indeed observed to accumulate not only in Hutchinson-Gilford progeria syndrome (HGPS) but also during normal aging. Studies have shown that progerin accumulation in HGPS patients is caused by LMNA gene mutations. Furthermore, research indicates that progerin accumulation during physiological aging contributes to multiple nuclear abnormalities. In the context of normal aging, progerin has been associated with the accumulation of genomic DNA double-strand breaks, leading to altered DNA repair mechanisms. This suggests that progerin plays a role in both premature aging syndromes like HGPS and in the natural aging process by impacting cellular functions and genomic stability.

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