Ge Zhang's research while affiliated with University of Central Florida and other places
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Publications (13)
Bim is a BH3-only member of the Bcl-2 family that enables the death of T-cells. Partial rescue of cytokine-deprived T-cells occurs when Bim and the receptor for the T-cell growth factor, interleukin-7, are deleted, implicating Bim as a possible target of interleukin-7-mediated signaling. Alternative splicing yields three major isoforms: BimEL, BimL...
The Bcl-2 family proteins maintain the balance of life and death in a cell. Bax, a pro-apoptotic member, translocates to the mitochondrial membrane in response to diverse death stimuli, initiating a cascade of programmed events that lead to cell death. Tumor progression involves deregulation of this process, in part, through mutations that cause ab...
Defects in the apoptotic machinery can contribute to tumor formation and resistance to treatment, creating a need to identify new agents that kill cancer cells by alternative mechanisms. To this end, we examined the cytotoxic properties of a novel peptide, CT20p, derived from the C-terminal, alpha-9 helix of Bax, an amphipathic domain with putative...
Interleukin-7 (IL-7) is an essential cytokine for lymphocyte growth that has the potential for promoting immune reconstitution. This feature makes IL-7 an ideal candidate for therapeutic development. As with other cytokines, signaling through the IL-7 receptor induces the JAK/STAT pathway. However, the broad scope of IL-7 regulatory targets likely...
STAT5 does not promote HXKII gene expression or glucose uptake in response to IL-7. (A, B) D1 cells were nucleofected with pcDNA (empty vector) or constitutively active STAT5a-CA (A) and evaluated for HXKII gene expression using quantitative PCR or (B) glucose uptake as described in Methods. Results are representative of two independent experiments...
Identified JunD target genes in the three cell lines. JunD-regulated gene targets were identified by ChIP-seq as described in Methods. The top three most significant gene ontology terms that are at least at level 5 for each group of target genes are provided when they are available. For each term, a gene ontology term ID is provided, followed by th...
The list of target genes in the three cell lines and their shared function shown in Figure S2 are provided in the supplemental file.
(XLS)
The dual functionality of the tumor suppressor, BAX, is implied by the non-apoptotic functions of other pro-apoptotic BCL-2 family proteins. To explore this, the mitochondrial morphology and ATP producing capability in both BAX-containing and BAX-deficient HCT-116 colon cancer cells were examined. While BAX deficient cells maintain the same mitocho...
The dual functionality of the tumor suppressor BAX is implied by the nonapoptotic functions of other members of the BCL-2 family. To explore this, mitochondrial metabolism was examined in BAX-deficient HCT-116 cells as well as primary hepatocytes from BAX-deficient mice. Although mitochondrial density and mitochondrial DNA content were the same in...
Apoptosis is a complex process essential for cellular homeostasis. Early physiological changes that initiate cell death remain poorly understood. Previously, we observed that lymphocytes, undergoing apoptosis in response to loss of a growth factor experienced a rapid rise in cytosolic pH. We found that the protein responsible was the Na+/H+ Exchang...
Apoptosis is a complex process essential for normal tissue development and cellular homeostasis. While biochemical events that occur late in the apoptotic process are better characterized, early physiological changes that initiate the progression of cell death remain poorly understood. Previously, we observed that lymphocytes, undergoing apoptosis...
Apoptosis is essential for lymphocyte development and the maintenance of cellular homeostasis. Previously, we showed that the apoptotic protein, BAX, is a critical mediator of IL-7-withdrawal induced death; yet, how this deadly protein is activated is poorly understood. Under apoptotic stress, BAX translocates to mitochondria, causing cell death. T...
Citations
... In particular, BIML can directly neutralize Bcl-xL to promote apoptosis by Bax activation 53 . BIML has also been related to cell maintenance or autophagic activities, through its interaction with dynein which facilitates the loading, fusion, and positioning of lysosomes 54 . Moreover, a previous study demonstrated that pro-apoptotic protein fragments Asp-Bcl-xL, Arg-Bid, and Arg-BIMEL are short-lived substrates by selective degradation of the N-degron pathway, which contributes to preventing the pro-apoptotic signal from reaching the point of commitment of apoptosis 55 . ...
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... NP were synthesized and encapsulated with cargo as described previously (33). NP were loaded with either 1,1'-Dioctadecyl-3,3,3',3'-Tetramethylindo carbocyanine Perchlorate (DiI dye) (ThermoFisher) or CT20p (Acetyl -VTIFVAGVLTASLTIWKKMG -Amine) peptide (Biopeptide Inc) as previously described (33,34). DiI-loaded NP (0.02-0.1 mg) was used to assess uptake by IMR-32 cells and to detect any non-specific toxicity associated with NP carrier. ...
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... Tools like NicheNet, PyMINEr and scMLnet fall into the pathway-involved category, while others are majorly non-pathway-involved. The pathway-involved tools are primarily motivated by the essential role of intracellular signaling and transcriptional regulation events during CCIs [12,26,71,72]. Therefore, these tools take into account the signaling pathway components by performing pathway integration and analysis when inferring LR interactions and CCIs. ...
... Suppression or elimination of Bax and Bak proteins was reported to impose various effects on mitochondrial respiration. Bax-deficient HCT-116 cells and mouse hepatocytes showed attenuated mitochondrial respiration, lower levels of ATP and increased glycolysis [34]. In contrast, another report documented direct interaction of Bax and Bak with mtND5, mitochondrial DNA (mtDNA)-encoded subunit of CI, attenuating CI activity and mitochondrial respiration in lung and colorectal cancer cells [35]. ...
... This may be a possible interpretation that chronic myeloid leukemia (CML) and other hematopoietic malignances resist apoptosis resulting from DNA damage. NHE1, a highly conserved plasma membrane protein well established, regulate cell migration [10], proliferation [11], and death [9,12] through the extrusion of intracellular proton (H + ) in exchange for extracellular sodium (Na + ) [13]. Increased NHE1 activity and/or expression has been shown in a variety of cancer types, including several breast cancer cell types [14], and has been proposed to be an early event in transformation especially via increased survival [15] and migratory/invasive properties [10]. ...
