p130, p107, and pRb Are Differentially Regulated in Proliferating Cells and during Cell Cycle Arrest by α-Interferon

Thomas, N. Shaun B.; Pizzey, Arnold; Tiwari, Sanjay; Williams, Catherine; Yang, Jiewu

doi:10.1074/jbc.273.37.23659

Cited by 49 publications

(62 citation statements)

References 67 publications

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“…We have shown previously that pRb is phosphorylated by cdk6 or cdk4-cyclin D2 early during the transition of human primary T cells from G 0 to early G 1 (G 1 A) (67). Phosphorylation of pRb at cdk6/4-cyclin D specific sites does not occur in T cells stimulated in the presence of AML cells, which is consistent with a block in cell cycle progression very early during the G 0 to G 1 A transition.…”

Section: Discussionsupporting

confidence: 49%

Microenvironment Produced by Acute Myeloid Leukemia Cells Prevents T Cell Activation and Proliferation by Inhibition of NF-κB, c-Myc, and pRb Pathways

Buggins¹,

Milojković²,

Arno³

et al. 2001

The Journal of Immunology

133

113

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Tumors produce a variety of immunosuppressive factors which can prevent the proliferation and maturation of a number of normal hemopoietic cell types. We have investigated whether primary acute myeloid leukemia (AML) cells have an effect on normal T cell function and signaling. Tumor cell supernatant (TSN) from AML cells inhibited T cell activation and Th1 cytokine production and also prevented activated T cells from entering the cell cycle. These effects occurred in the absence of AML cell-T cell contact. We have demonstrated that AML TSN contained none of the immunosuppressors described to date, namely gangliosides, nitric oxide, TGF-β, IL-10, vascular endothelial growth factor, or PGs. Furthermore, IL-2 did not overcome the block, despite normal IL-2R expression. However, the effect was overcome by preincubation with inhibitors of protein secretion and abolished by trypsinization, indicating that the active substance includes one or more proteins. To determine the mechanism of inhibition, we have studied many of the major pathways involved in T cell activation and proliferation. We show that nuclear translocation of NFATc and NF-κB are markedly reduced in T cells activated in the presence of primary AML cells. In contrast, calcium mobilization and activation of other signal transduction pathways, namely extracellular signal-regulated kinase1/2, p38, and STAT5 were unaffected, but activation of c-Jun N-terminal kinase 1/2 was delayed. Phosphorylation of pRb by cyclin-dependent kinase 6/4-cyclin D and of p130 did not occur and c-Myc, cyclin D3, and p107 were not induced, consistent with cell cycle inhibition early during the transition from G0 to G1. Our data indicate that TSN generated by AML cells induces T cell immunosuppression and provides a mechanism by which the leukemic clone could evade T cell-mediated killing.

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Section: Discussionsupporting

confidence: 49%

Microenvironment Produced by Acute Myeloid Leukemia Cells Prevents T Cell Activation and Proliferation by Inhibition of NF-κB, c-Myc, and pRb Pathways

Buggins¹,

Milojković²,

Arno³

et al. 2001

The Journal of Immunology

133

113

View full text Add to dashboard Cite

show abstract

“…In most cases, the critical transcription factor mediating the IFN effects had not been identified. Some of these gene products, such as RAC-2 and p130 (Rb related), are modulated by type I IFNs (60,87). The p8 protein codes for a homologue of a bovine chemokine (85).…”

Section: Methodsmentioning

confidence: 99%

Critical Role for Transcription Factor C/EBP-β in Regulating the Expression of Death-Associated Protein Kinase 1

Gade

Roy

et al. 2008

Molecular and Cellular Biology

102

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“…This allows for an optimal recovery of these proteins at the purification stage. The following is a sample of papers that used this protocol to recover biotinylated proteins: [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25]. Following the pre-adsorption phase, the column was then washed with 16 ml of 10 % acetic acid and 0.1 M NaHPO 4 until the pH of the flow-through was >6.8.…”

Section: Biotin Avidin Columnmentioning

confidence: 99%

What maintains the high intra-follicular estradiol concentration in pre-ovulatory follicles?

Bentov

Jurisicova

Kenigsberg

et al. 2015

J Assist Reprod Genet

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Purpose The purpose of the study was to establish the mechanism by which the estrogen concentration difference between the follicular fluid and the serum is maintained. Methods We used dialysis membrane with a pore size of <3 KD to characterize the estrogen-binding capacity of the follicular fluid. We performed PCR, western blot, and ELISA on luteinized granulosa cells to determine if sex hormonebinding globulin (SHBG) is produced by granulosa cells, and finally we used affinity columns and mass spectrometry to identify the estrogen-binding protein in the follicular fluid. Results We found that a significant estrogen concentration difference is maintained in a cell-free system and is lost with proteolysis of the follicular fluid proteins. Luteinized granulosa cells are likely not a source of SHBG, as we were not able to detect expression of SHBG in these cells. Perlecan was the most highly enriched follicular fluid protein in the affinity columns. Conclusions We were able to identify perlecan as the most likely candidate for the major estrogen-binding protein in the follicular fluid.

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p130, p107, and pRb Are Differentially Regulated in Proliferating Cells and during Cell Cycle Arrest by α-Interferon

Cited by 49 publications

References 67 publications

Microenvironment Produced by Acute Myeloid Leukemia Cells Prevents T Cell Activation and Proliferation by Inhibition of NF-κB, c-Myc, and pRb Pathways

Microenvironment Produced by Acute Myeloid Leukemia Cells Prevents T Cell Activation and Proliferation by Inhibition of NF-κB, c-Myc, and pRb Pathways

Critical Role for Transcription Factor C/EBP-β in Regulating the Expression of Death-Associated Protein Kinase 1

What maintains the high intra-follicular estradiol concentration in pre-ovulatory follicles?

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