scholarly journals BDNF splice variants from the second promoter cluster support cell survival of differentiated neuroblastoma upon cytotoxic stress

2008 ◽  
Vol 122 (1) ◽  
pp. 36-43 ◽  
Author(s):  
B. Gabriele ◽  
T. Enrico
Keyword(s):  
Cell Survival ◽  
Splice Variants ◽  
Support Cell ◽  
Cytotoxic Stress ◽  
Promoter Cluster

scholarly journals Hepatitis C virus NS 5A drives a PTEN ‐ PI 3K/Akt feedback loop to support cell survival

2014 ◽  
Vol 35 (6) ◽  
pp. 1682-1691 ◽  
Author(s):  
Du Cheng ◽  
Leiliang Zhang ◽  
Guangbo Yang ◽  
Lei Zhao ◽  
Feng Peng ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Survival ◽  
Feedback Loop ◽  
Support Cell

Survival-promoting functions of 14-3-3 proteins

2002 ◽  
Vol 30 (4) ◽  
pp. 360-365 ◽  
Author(s):  
S. C. Masters ◽  
R. R. Subramanian ◽  
A. Truong ◽  
H. Yang ◽  
K. Fujii ◽  
...  
Keyword(s):  
Cell Survival ◽  
Anticancer Agents ◽  
Cellular Proteins ◽  
Support Cell ◽  
Antagonist Peptides ◽  
Ligand Interactions ◽  
Cellular Machinery ◽  
In Cells

The 14-3-3 proteins are a family of phosphoserine/phosphothreonine-binding molecules that control the function of a wide array of cellular proteins. We suggest that one function of 14-3-3 is to support cell survival. 14-3-3 proteins promote survival in part by antagonizing the activity of associated proapoptotic proteins, including Bad and apoptosis signal-regulating kinase 1 (ASK1). Indeed, expression of 14-3-3 inhibitor peptides in cells is sufficient to induce apoptosis. Interestingly, these 14-3-3 antagonist peptides can sensitize cells for effective killing by anticancer agents such as cisplatin. Thus, 14-3-3 may be part of the cellular machinery that maintains cell survival, and targeting 14-3-3-ligand interactions may be a useful strategy to enhance the efficacy of conventional anticancer agents.

scholarly journals GRP78 enhances the glutamine metabolism to support cell survival from glucose deficiency by modulating the β-catenin signaling

Oncotarget ◽  
2014 ◽  
Vol 5 (14) ◽  
pp. 5369-5380 ◽  
Author(s):  
Zongwei Li ◽  
Yingying Wang ◽  
Haili Wu ◽  
Lichao Zhang ◽  
Peng Yang ◽  
...  
Keyword(s):  
Cell Survival ◽  
Glutamine Metabolism ◽  
Support Cell

scholarly journals IG20, in contrast to DENN-SV, (MADD splice variants) suppresses tumor cell survival, and enhances their susceptibility to apoptosis and cancer drugs

Oncogene ◽  
2004 ◽  
Vol 23 (5) ◽  
pp. 1076-1087 ◽  
Author(s):  
Elena V Efimova ◽  
Adeeb M Al-Zoubi ◽  
Osvaldo Martinez ◽  
Shashi Kaithamana ◽  
Shenfeng Lu ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Survival ◽  
Splice Variants ◽  
Cancer Drugs ◽  
Tumor Cell Survival

scholarly journals Evaluation of the Role of Human DNAJAs in the Response to Cytotoxic Chemotherapeutic Agents in a Yeast Model System

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Aurellia Whitmore ◽  
Devon Freeny ◽  
Samantha J. Sojourner ◽  
Jana S. Miles ◽  
Willie M. Graham ◽  
...  
Keyword(s):  
Heat Shock ◽  
Cell Survival ◽  
Cellular Response ◽  
Chemotherapeutic Agents ◽  
Dna Double Strand Breaks ◽  
Anthracycline Antibiotics ◽  
First Line Therapy ◽  
Development Of Resistance ◽  
Cytotoxic Stress

Heat-shock proteins (HSPs) play a crucial role in maintaining protein stability for cell survival during stress-induced insults. Overexpression of HSPs in cancer cells results in antiapoptotic activity contributing to cancer cell survival and restricting the efficacy of cytotoxic chemotherapy, which continues to play an important role in the treatment of many cancers, including triple-negative breast cancer (TNBC). First-line therapy for TNBC includes anthracycline antibiotics, which are associated with serious dose-dependent side effects and the development of resistance. We previously identified YDJ1, which encodes a heat-shock protein 40 (HSP40), as an important factor in the cellular response to anthracyclines in yeast, with mutants displaying over 100-fold increased sensitivity to doxorubicin. In humans, the DNAJA HSP40s are homologues of YDJ1. To determine the role of DNAJAs in the cellular response to cytotoxic drugs, we investigated their ability to rescue ydj1Δ mutants from exposure to chemotherapeutic agents. Our results indicate that DNAJA1 and DNAJA2 provide effective protection, while DNAJA3 and DNAJA4 did not. The level of complementation was also dependent on the agent used, with DNAJA1 and DNAJA2 rescuing the ydj1Δ strain from doxorubicin, cisplatin, and heat shock. DNAJA3 and DNAJA4 did not rescue the ydj1Δ strain and interfered with the cellular response to stress when expressed in wild type background. DNAJA1 and DNAJA2 protect the cell from proteotoxic damage caused by reactive oxygen species (ROS) and are not required for repair of DNA double-strand breaks. These data indicate that the DNAJAs play a role in the protection of cells from ROS-induced cytotoxic stress.

scholarly journals Extracellular Vesicles Support the Survival of Serum-dependent cells in vitro

2020 ◽  
Vol 21 (2) ◽  
Author(s):  
Christy Mikhael ◽  
Shannon Holliday ◽  
Guanghong Han
Keyword(s):  
Cell Survival ◽  
Extracellular Vesicles ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Support Cell ◽  
Cell Counts ◽  
4T1 Cells ◽  
Serum Dependent ◽  
Extracellular Environment

Extracellular vesicles (EVs) are 30-150 nm in diameter and are released by cells into the extracellular environment. They facilitate intercellular communication and may be involved in cell survival. Although serum-dependent cells are not obviously affected by depletion of EVs from the serum, we previously reported that cells in serum that contain EVs were more resistant to the drugs, enoxacin and bis-enoxacin, compared to cells in serum without EVs. This change in resistance led us to examine whether EVs are sufficient to maintain serum dependent cells in vitro. Here, we tested the effect of EVs on the survival RAW 264.7 cells and on 4T1 murine breast cancer cells. EVs were isolated by differential centrifugation. EVs were counted over various time periods. Cells were grown in alpha or Dulbecco’s minimal essential media supplemented with FBS, EVs from various sources, or with no supplements. Cell growth was determined by cell counts. In media without supplementation, the RAW 264.7 cells and 4T1 cells died by three days. Media supplemented with EVs from FBS allowed the cells to survive in the absence of FBS for one week or more.  Being able to perform experiments on cells supported by EVs will simplify the interpretation of experiments. Efforts are underway to determine their mechanism by which EVs support cell survival.

scholarly journals Impact of the MDM2 splice-variants MDM2-A, MDM2-B and MDM2-C on cytotoxic stress response in breast cancer cells

2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Johanna Huun ◽  
Liv B. Gansmo ◽  
Bård Mannsåker ◽  
Gjertrud Titlestad Iversen ◽  
Jan Inge Øvrebø ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stress Response ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Splice Variants ◽  
Cytotoxic Stress

The AP-2 transcription factor is required for joint formation and cell survival in Drosophila leg development

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1231-1238 ◽  
Author(s):  
B. Kerber ◽  
I. Monge ◽  
M. Mueller ◽  
P.J. Mitchell ◽  
S.M. Cohen
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Notch Signaling ◽  
Cell Survival ◽  
Leg Length ◽  
Notch Activity ◽  
Support Cell ◽  
Important Mediator ◽  
Leg Development ◽  
Severe Reduction

Flies mutant for the Drosophila homologue of the mammalian transcription factor AP-2 show a severe reduction in leg length and fail to develop joint structures. Presumptive joint cells express dAP-2 in response to Notch signaling. dAP-2 is required for joint cell differentiation and can induce formation of supernumerary joints when misexpressed. Although dAP-2 is expressed only in presumptive joint cells, its activity is required to support cell survival in the entire leg segment. Taken together, our data indicate that dAP-2 is an important mediator of Notch activity in leg development.

scholarly journals A Naturally Occurring Splice Variant of CXCL12/Stromal Cell-Derived Factor 1 Is a Potent Human Immunodeficiency Virus Type 1 Inhibitor with Weak Chemotaxis and Cell Survival Activities

2007 ◽  
Vol 81 (15) ◽  
pp. 8140-8148 ◽  
Author(s):  
Jeffrey D. Altenburg ◽  
Hal E. Broxmeyer ◽  
Qingwen Jin ◽  
Scott Cooper ◽  
Sunanda Basu ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cell Survival ◽  
Stromal Cell ◽  
Splice Variants ◽  
Biological Properties ◽  
Affinity Column ◽  
Immunodeficiency Virus ◽  
Antiviral Activities ◽  
Stromal Cell Derived Factor

ABSTRACT CXCL12/stromal cell-derived factor 1 is a member of the CXC family of chemokines that plays an important role in hematopoiesis and signals through CXCR4 and CXCR7. Two splice variants of human CXCL12 (CXCL12α and CXCL12β) induce chemotaxis of CXCR4+ cells and inhibit X4 infection. Recent studies described four other novel splice variants of human CXCL12; however, their antiviral activities were not investigated. We constructed and expressed all of the CXCL12 splice variants in Escherichia coli. Recombinant proteins were purified through a His affinity column, and their biological properties were analyzed. All six CXCL12 variants induced chemotaxis of CXCR4+ and CXCR7+ cell lines. Enhancement of survival and replating capacity of human hematopoietic progenitor cells were observed with CXCL12α, CXCL12β, and CXCL12ε but not with the other variants. CXCL12γ showed the greatest antiviral activity in X4 inhibition assays and the weakest chemotaxis activity through CXCR4. The order of potency in X4 inhibition assays was as follows: CXCL12γ > CXCL12β > CXCL12α > CXCL12θ > CXCL12ε > CXCL12δ. The order of anti-human immunodeficiency virus (HIV) activity was associated with the number of BBXB motifs present in each variant; the most potent inhibitor was CXCL12γ, with five BBXB domains. The results suggest that the different C termini of CXCL12 variants may contain important molecular determinants for the observed differences in antiviral effects and other biological functions. These studies implicate CXCL12γ as a potent HIV-1 entry inhibitor with significantly reduced chemotaxis activity and small or absent effects on progenitor cell survival or replating capacity, providing important insight into the structure-function relationships of CXCL12.

Sign in / Sign up

Export Citation Format

Share Document