Identification and characterization of mouse PSF1-binding protein, SLD5

Kong, Lingyu; Ueno, Masaya; Itoh, Machiko; Yoshioka, Katsuji; Takakura, Nobuyuki

doi:10.1016/j.bbrc.2005.11.136

Cited by 14 publications

(13 citation statements)

References 13 publications

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“…23 GAPDH was detected with anti-GAPDH antibodies (Chemicon International, Temecula, CA) for endogenous protein control. Transfection efficiency of each plasmid was determined by qRT-PCR (see "qRT-PCR").…”

Section: Transfection and Immunoblot Analysismentioning

confidence: 99%

Both alleles of PSF1 are required for maintenance of pool size of immature hematopoietic cells and acute bone marrow regeneration

Ueno

Itoh

Sugihara

et al. 2009

Blood

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Hematopoietic stem cells (HSCs) have a very low rate of cell division in the steady state; however, under conditions of hematopoietic stress, these cells can begin to proliferate at high rates, differentiate into mature hematopoietic cells, and rapidly reconstitute ablated bone marrow (BM). Previously, we isolated a novel evolutionarily conserved DNA replication factor, PSF1 (partner of SLD5-1), from an HSCspecific cDNA library. In the steady state,

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Section: Transfection and Immunoblot Analysismentioning

confidence: 99%

Both alleles of PSF1 are required for maintenance of pool size of immature hematopoietic cells and acute bone marrow regeneration

Ueno

Itoh

Sugihara

et al. 2009

Blood

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“…The GINS complex plays an essential role in the initiation of DNA replication and progression of DNA replication forks (Takayama et al, 2003). SLD5 is important for GINS complex assembly (Aparicio et al, 2009;Kong et al, 2006). Thus, we next determined whether SLD5 is essential for DNA replication.…”

Section: Cellular Dna Replication Is Blocked By Knockdown or Mutatimentioning

confidence: 99%

“…One of the candidate proteins that we identified is SLD5, which is one component of the GINS complex and plays a central role in this complex (Kong, Ueno, Itoh, Yoshioka, & Takakura, 2006;Takayama et al, 2003). One of the candidate proteins that we identified is SLD5, which is one component of the GINS complex and plays a central role in this complex (Kong, Ueno, Itoh, Yoshioka, & Takakura, 2006;Takayama et al, 2003).…”

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confidence: 97%

“…In order to fully explore host factors that physically interact with M1, we constructed a yeast two-hybrid library derived from the lung tissue of C57BL/6 mice, then used M1 as the bait to search for possible counterpart host proteins. One of the candidate proteins that we identified is SLD5, which is one component of the GINS complex and plays a central role in this complex (Kong, Ueno, Itoh, Yoshioka, & Takakura, 2006;Takayama et al, 2003). The formation of GINS complex is essential for the initiation of DNA replication (Aparicio, Guillou, Coloma, Montoya, & Mendez, 2009;Chang, Wang, Bermudez, Hurwitz, & Chen, 2007;Choi, Lim, Kim, Song, & Cho, 2007;Kamada, Kubota, Arata, Shindo, & Hanaoka, 2007;Labib & Gambus, 2007;Moyer, Lewis, & Botchan, 2006;Pacek, Tutter, Kubota, Takisawa, & Walter, 2006).…”

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confidence: 99%

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Influenza virus matrix protein M1 interacts with SLD5 to block host cell cycle

Zhu

Zhao

et al. 2019

Cellular Microbiology

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Influenza virus matrix 1 protein (M1) is highly conserved and plays essential roles at many stages of virus life cycle. Here, we used a yeast two-hybrid system to identify the host protein SLD5, a component of the GINS complex, which is essential for the initiation of DNA replication in eukaryotic cells, as a new M1 interacting protein. M1 from several different influenza virus strains all interacted with SLD5. Overexpression of SLD5 suppressed influenza virus replication. Transient, stable, or inducible expression of M1 induced host cell cycle blockade at G0/G1 phase. Moreover, SLD5 partially rescued M1 expression-or influenza virus infection-induced G0/G1 phase accumulation in cell lines and primary mouse embryonic fibroblasts. Importantly, SLD5 transgenic mice exhibited higher resistance and improved lung epithelial regeneration after virus infection compared with wild-type mice. Therefore, influenza virus M1 blocks host cell cycle process by interacting with SLD5. Our finding reveals the multifunctional nature of M1 and provides new insight for understanding influenza virus-host interaction.

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“…Procedures for the preparation of cell lysates and western blotting were basically the same as those reported previously. ( 11 ) Briefly, total protein was extracted using Nonidet (N)P‐40 Tris buffer with proteinase inhibitor cocktail added. Proteins were fractioned by sodium dodecylsulfate–polyacrylamide gel electrophoresis and transferred to a membrane.…”

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confidence: 99%

Inhibition of axonal outgrowth in the tumor environment: Involvement of class 3 semaphorins

et al. 2007

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That tumors lack innervation is dogma in the field of pathology, but the molecular determinants of this phenomenon remain elusive. We studied the effects of conditioned media from Colon 26 and B16 mouse tumor cell lines on the axonal outgrowth and cellular differentiation of embryonic Institute of Cancer Research (ICR) mouse dorsal root ganglion cells. Tumor-conditioned media suppressed dorsal root ganglion axonal extension but had no effect on neuronal or glial differentiation. We found that the tumor cells expressed most of the class 3 semaphorins -axon guidance molecules. T he lack of innervation in tumors is a generally accepted fact,(1) but the molecular determinants of this phenomenon are poorly understood. Furthermore, certain tumors such as esophageal cancer were shown to be innervated by peptidergic nerve fibers and to promote process extension in DRG neurons. (2) Notably, sarcomas can secrete NGF, which promotes proliferation and axonal outgrowth of DRG neurons, the observation of which led to the initial discovery of NGF.(3) Thus, the effects of tumors on axonal growth are unclear and need further analysis.Peripheral nerves are known to associate with blood vessels,reflecting their need for oxygen and nutrients and their control of vasoconstriction and vasodilation. (5) In mutant embryos containing disorganized nerves, blood vessel branching is altered to follow the nerve, (6) suggesting that local signals supplied by nerve fibers may provide a template that determines blood vessel patterning. These data indicate a functional relationship between axonal outgrowth and angiogenesis under physiological conditions, and make the question of tumor innervation even more intriguing.DRG neurons innervate most of the internal organs, thus their processes have the highest potential for interacting with the cells of a tumor growing in the body. We therefore investigated whether molecular cues secreted from tumor cells affect axonal outgrowth and additionally alter the differentiation capacity of immature neural cells in the DRG. Here, we report that supernatant isolated from two tumor cell line cultures inhibited process extension of DRG neurons, and present evidence implicating secreted class 3 semaphorins as mediators of this tumor-induced axonal inhibition. Materials and MethodsDRG culture. Embryos at embryonic day 12.5 were dissected from pregnant Institute of Cancer Research (ICR) mice (SCL, Shizuoka, Japan). DRG were extracted free of surrounding tissues and placed one per well in 24-well, poly-l-lysine-coated culture plates (Iwaki, Tokyo, Japan). Colon 26 (C26; mouse colon cancer) and B16 (mouse melanoma) tumor cell lines were cultured in DMEM (Sigma-Aldrich, St Louis, MO, USA) supplemented with 10% FBS (Sigma-Aldrich). Culture supernatants were collected when cells reached approximately 80% confluence. Four culture media were prepared: (i) control medium, DMEM + 10% FBS + 50 ng/mL human recombinant NGF (PeproTech, Rocky Hill, NJ, USA); (ii) tumor-conditioned medium, equal amounts of control medium with 10...

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Identification and characterization of mouse PSF1-binding protein, SLD5

Cited by 14 publications

References 13 publications

Both alleles of PSF1 are required for maintenance of pool size of immature hematopoietic cells and acute bone marrow regeneration

Both alleles of PSF1 are required for maintenance of pool size of immature hematopoietic cells and acute bone marrow regeneration

Influenza virus matrix protein M1 interacts with SLD5 to block host cell cycle

Inhibition of axonal outgrowth in the tumor environment: Involvement of class 3 semaphorins

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