The volcanic relationship of model phthalocyanine molecular catalysts in the CO reduction reaction.

We have constructed a series of model metal phthalocyanines (MPc) for the carbon dioxide reduction reaction (CORR), constructed a volcano relationship through density functional theory (DFT) and experiments, and obtained cobalt phthalocyanine (CoPc) at the apex. The volcano diagram is conducive to the screening of catalysts and has a guiding role in the design of catalysts.

Corrigendum: Bovine Pre-adipocyte Adipogenesis Is Regulated by bta-miR-150 Through mTOR Signaling.

[This corrects the article DOI: 10.3389/fgene.2021.

Bovine Pre-adipocyte Adipogenesis Is Regulated by bta-miR-150 Through mTOR Signaling.

Micro RNA (miR) are recognized for their important roles in biological processes, particularly in regulatory componentization. Among the miR, miR-150 has been the focus of intense scrutiny, mostly due to its role in malignant tumors. A comparison between steer and bull adipose tissues identified bta-miR-150 as one of the nine downregulated miRNAs, although its function remains unknown (GEO:GSE75063).

Treatment of esophageal cancer with multiple liver metastases: a case experience of sustained complete response.

Esophageal squamous cell cancer with distant metastases has a poor prognosis. The metastatic sites usually involve the liver, bones, and lungs. Treatment of metastatic disease is essentially palliative and based on chemoradiotherapy.

REDD1 Is Essential for Optimal T Cell Proliferation and Survival.

REDD1 is a highly conserved stress response protein that is upregulated following many types of cellular stress, including hypoxia, DNA damage, energy stress, ER stress, and nutrient deprivation. Recently, REDD1 was shown to be involved in dexamethasone induced autophagy in murine thymocytes. However, we know little of REDD1's function in mature T cells.

Co-expression of CD40/CD40L on XG1 multiple myeloma cells promotes IL-6 autocrine function.

Multiple myeloma (MM) is characterized by uncontrolled proliferation of malignant plasma cells in the bone marrow and peripheral blood. Here, we found that CD40 and CD40L co-expressed on XG1 MM cells and the coordinated expression of CD40-CD40L was critical for production and autocrine IL-6 in XG1 cells. Furthermore, TNF-α enhanced the expression of both CD40 and CD40L expression on XG1 cells.

HIV-1 Vif promotes the G₁- to S-phase cell-cycle transition.

HIV-1 depends on host-cell resources for replication, access to which may be limited to a particular phase of the cell cycle. The HIV-encoded proteins Vpr (viral protein R) and Vif (viral infectivity factor) arrest cells in the G₂ phase; however, alteration of other cell-cycle phases has not been reported. We show that Vif drives cells out of G₁ and into the S phase.

The HIV-1 Vif protein mediates degradation of Vpr and reduces Vpr-induced cell cycle arrest.

Prior work has implicated viral protein R (Vpr) in the arrest of human immunodeficiency virus type 1 (HIV-1)-infected cells in the G2 phase of the cell cycle, associated with increased viral replication and host cell apoptosis. We and others have recently shown that virion infectivity factor (Vif ) also plays a role in the G2 arrest of HIV-1-infected cells. Here, we demonstrate that, paradoxically, at early time points postinfection, Vif expression blocks Vpr-mediated G2 arrest, while deletion of Vif from the HIV-1 genome leads to a marked increase in G2 arrest of infected CD4 T-cells.

The Vif accessory protein alters the cell cycle of human immunodeficiency virus type 1 infected cells.

The viral infectivity factor gene (vif) of HIV-1 increases the infectivity of viral particles by inactivation of cellular anti-viral factors, and supports productive viral replication in primary human CD4 T cells and in certain non-permissive T cell lines. Here, we demonstrate that Vif also contributes to the arrest of HIV-1 infected cells in the G(2) phase of the cell cycle. Viruses deleted in Vif or Vpr induce less cell cycle arrest than wild-type virus, while cells infected with HIV-1 deleted in both Vif and Vpr have a cell cycle profile equivalent to that of uninfected cells.

Sensitization of multiple myeloma and B lymphoma lines to dexamethasone and gamma-radiation-induced apoptosis by CD40 activation.

We examined the effects of CD40 activation with dexamethasone (Dex) or 60Co-gamma-irradiation on the growth of malignant B cells in vitro, using the human multiple myeloma (MM) cell line, XG2, and the B lymphoma Daudi cell line as models. Both lines are resistant to Dex and irradiation; 10(-7)M Dex or 10 Gy of gamma-irradiation induced only minimal growth arrest and apoptosis of the cells. Treatment of the cells with the agonistic anti-CD40 monoclonal antibody 5C11 partially inhibited the proliferation of the Daudi cells; XG2 underwent apoptosis.

CXCR4 engagement is required for HIV-1-induced L-selectin shedding.

The chemokine receptor, CXCR4, serves as the primary coreceptor for entry of T-cell tropic human immunodeficiency virus (HIV). Binding of either the CXC-chemokine, stromal-derived factor 1 alpha (SDF-1 alpha), or a CXCR4 antagonist, AMD3100, to CXCR4 inhibits infection of CD4(+) T cells by T-tropic HIV-1, although only SDF-1 alpha triggers T-cell signaling cascades. We have previously demonstrated that ligation of CD4 by T-cell tropic HIV-1 NL4-3 induces metalloproteinase-dependent L-selectin (CD62L) shedding on resting CD4(+) T cells.

T cell signaling and apoptosis in HIV disease.

Groundbreaking research has led to an understanding of some of the pathogenic mechanisms of HIV-1 infection. Surprisingly, an unanswered question remains the mechanism(s) by which HIV-1 inactivates or kills T cells. Our goals are to define candidate T cell signaling cascades altered by HIV infection and to identify mechanisms whereby HIV-infected cells escape the apoptosis triggered by this aberrant signaling.