Assignment of the 49-kDa (PRIM1) and 58-kDa (PRIM2A and PRIM2B) Subunit Genes of the Human DNA Primase to Chromosome Bands 1q44 and 6p11.1-p12

Shiratori, Akiko; Okumura, Katsuhiko; Nogami, Masahiro; Taguchi, Hiroshi; Onozaki, Tokiro; Inoue, Tadashi; Ando, Toshiaki; Shibata, Takehiko; Izumi, Masako; Miyazawa, Hiroshi; Hanaoka, Fumio; Murakami, Yasufumi; Eki, Toshihiko

doi:10.1006/geno.1995.1155

Cited by 30 publications

(27 citation statements)

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“…The protein encoded by UIMC1 physically interacts with BRCA1 and estrogen receptor α (ERα) and is thought to recruit BRCA1 to DNA damage sites and to initiate G2/M checkpoint control. PRIM1 (Primase) is involved in DNA replication by synthesising RNA primers for Okazaki fragments during discontinuous replication 35 . A mutation in POLG can segregate with primary ovarian insufficiency (POI) 36 .…”

Section: Discussionmentioning

confidence: 99%

Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways

Stolk¹,

Perry²,

Chasman³

et al. 2012

Nat Genet

330

327

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To identify novel loci for age at natural menopause, we performed a meta-analysis of 22 genome-wide association studies in 38,968 women of European descent, with replication in up to 14,435 women. In addition to four known loci, we identified 13 new age at natural menopause loci (P < 5 × 10−8). The new loci included genes implicated in DNA repair (EXO1, HELQ, UIMC1, FAM175A, FANCI, TLK1, POLG, PRIM1) and immune function (IL11, NLRP11, BAT2). Gene-set enrichment pathway analyses using the full GWAS dataset identified exodeoxyribonuclease, NFκB signalling and mitochondrial dysfunction as biological processes related to timing of menopause.

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Section: Discussionmentioning

confidence: 99%

Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways

Stolk¹,

Perry²,

Chasman³

et al. 2012

Nat Genet

330

327

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“…The following discussion is focused around the genes from this network for which expression was most affected by trisomy. The helicase minichromosome maintenance proteins (MCMs) and Prim1 (small subunit of primase, which synthesises oligoribonucleotides that act as primers for initiation of DNA synthesis) are involved in DNA replication and their reduced expression is likely to result in a delay or elongation of the S phase of the cell cycle [72], [73], [74]. Brca2 has various roles in the maintenance of genome stability, but its main function appears to involve the regulation of the function of Rad51 (DNA repair protein) during DNA repair by homologous recombination.…”

Section: Discussionmentioning

confidence: 99%

Gene Network Disruptions and Neurogenesis Defects in the Adult Ts1Cje Mouse Model of Down Syndrome

et al. 2010

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BackgroundDown syndrome (DS) individuals suffer mental retardation with further cognitive decline and early onset Alzheimer's disease.Methodology/Principal FindingsTo understand how trisomy 21 causes these neurological abnormalities we investigated changes in gene expression networks combined with a systematic cell lineage analysis of adult neurogenesis using the Ts1Cje mouse model of DS. We demonstrated down regulation of a number of key genes involved in proliferation and cell cycle progression including Mcm7, Brca2, Prim1, Cenpo and Aurka in trisomic neurospheres. We found that trisomy did not affect the number of adult neural stem cells but resulted in reduced numbers of neural progenitors and neuroblasts. Analysis of differentiating adult Ts1Cje neural progenitors showed a severe reduction in numbers of neurons produced with a tendency for less elaborate neurites, whilst the numbers of astrocytes was increased.Conclusions/SignificanceWe have shown that trisomy affects a number of elements of adult neurogenesis likely to result in a progressive pathogenesis and consequently providing the potential for the development of therapies to slow progression of, or even ameliorate the neuronal deficits suffered by DS individuals.

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“…The function of DNA primase is to synthesize the small RNA primers for Okazaki fragments generated during discontinuous DNA replication . DNA primase is also sometimes called RNA primase because it is a DNA‐dependent RNA polymerase.…”

Section: Introductionmentioning

confidence: 99%

DNA primase polypeptide 1 (PRIM1) involves in estrogen‐induced breast cancer formation through activation of the G2/M cell cycle checkpoint

Lee

Chen

Chia‐Jung

et al. 2018

Intl Journal of Cancer

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The DNA primase polypeptide 1 (PRIM1) is responsible for synthesizing small RNA primers for Okazaki fragments generated during discontinuous DNA replication. PRIM1 mRNA expression levels in breast tumor samples were detected by real-time PCR analysis. Xenografted tumor model was established to study the carcinogenic role of PRIM1 and its potential therapeutic applications. The average PRIM1 mRNA (copy number × 10 /μg) expression was 4.7-fold higher in tumors than in normal tissue (*p = 0.005, n = 254). PRIM1 was detected preferentially at a higher level (>40-fold) in poorly differentiated tumor tissues (n = 46) compared with more highly differentiated tumors tissues (n = 10) (*p = 0.005). Poor overall survival rate was correlated to the estrogen receptor positive (ER+, n = 20) patients with higher PRIM1 expression when compare to the ER- (n = 10) patients (Chi Square test, p = 0.03). Stable expression of PRIM1-siRNA in the ER+ BT-474 cells-xenograft tumors significantly reduced tumor volume in SCID mice (*p = 0.005). The anti-tumoral effects of inotilone isolated from Phellinus linteus was tested and had significant effects on the inhibition of PRIM1 protein expression in ER+ breast cancer cells. In vivo study was performed by administering inotilone (10 mg/kg, twice a week for 6 weeks), which resulted in significantly reduced BT-474-xenografted tumor growth volume compared with control (n =5 per group, *p < 0.05). This study provides evidences for the prognostic effects of PRIM1 with poor overall survival rate in the ER+ patients and will be valuable to test for therapeutic purpose.

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Assignment of the 49-kDa (PRIM1) and 58-kDa (PRIM2A and PRIM2B) Subunit Genes of the Human DNA Primase to Chromosome Bands 1q44 and 6p11.1-p12

Cited by 30 publications

References 0 publications

Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways

Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways

Gene Network Disruptions and Neurogenesis Defects in the Adult Ts1Cje Mouse Model of Down Syndrome

DNA primase polypeptide 1 (PRIM1) involves in estrogen‐induced breast cancer formation through activation of the G2/M cell cycle checkpoint

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