A5063118434- Cancer-related Molecular Pathways
- Inflammatory mediators and NSAID effects
- Virus-based gene therapy research
- Cancer, Stress, Anesthesia, and Immune Response
- Cancer Research and Treatments
- Helicobacter pylori-related gastroenterology studies
- Estrogen and related hormone effects
- NF-κB Signaling Pathways
- RNA Interference and Gene Delivery
- Cell death mechanisms and regulation
- Ubiquitin and proteasome pathways
- Drug Transport and Resistance Mechanisms
- Cytokine Signaling Pathways and Interactions
- Autophagy in Disease and Therapy
- Microtubule and mitosis dynamics
- interferon and immune responses
- Galectins and Cancer Biology
- Peptidase Inhibition and Analysis
- Cancer, Hypoxia, and Metabolism
- Adenosine and Purinergic Signaling
- Cancer Risks and Factors
- Advanced biosensing and bioanalysis techniques
- Immune Response and Inflammation
- Viral gastroenteritis research and epidemiology
- Biological Research and Disease Studies
Long Beach Medical Center
2003-2014
United States Department of Veterans Affairs
2005-2011
University of California, Irvine
2003-2007
VA Long Beach Healthcare System
2005
University of California, Berkeley
2000-2001
Rutgers, The State University of New Jersey
1994-1998
Adenovirus E1A expression recruits primary rodent cells into proliferation but fails to transform them because of the induction programmed cell death (apoptosis). The adenovirus E1B 19,000-molecular-weight protein (19K protein), 55K protein, and human Bcl-2 each cause high-frequency transformation when coexpressed with by inhibiting apoptosis. Thus, requires deregulation growth be coupled suppression product p53 tumor suppressor gene induces apoptosis in transformed is required for E1A....
Expression of the adenovirus E1A oncogene induces apoptosis which impedes both transformation primary rodent cells and productive infection human cells. Coexpression with E1B 19,000-molecular-weight protein (19K protein) or Bcl-2 protein, have antiapoptotic activity, is necessary for efficient transformation. Induction by in mediated p53 tumor suppressor gene, 19K can overcome this p53-dependent apoptosis. The functional similarity between suggested that they may act similar mechanisms...
BRK cell lines that stably express adenovirus E1A and a murine temperature-sensitive p53 undergo apoptosis when assumes the wild-type conformation.Expression of E1B 19,000-molecular-weight (19K) protein rescues cells from this p53-mediated diverts to growth-arrested state.As likely functions as tumor suppressor by regulating transcription, ability 19K regulate transactivation transcriptional repression was investigated.In promoter-reporter assays did not block but alleviate repression.E1B...
E1A expression during adenovirus infection induces apoptosis. causes accumulation of the p53 tumor suppressor protein, and E1A-induced apoptosis is mediated in primary rodent cells, implying that induction may be linked to by E1A. Adenoviruses containing mutations gene were tested for ability trigger both appearance enhanced cytopathy (cyt phenotype) degradation DNA (deg phenotype), indicative infected HeLa cells. The adenoviruses had which disrupted pRb- and/or p300-binding activities so...
Adenovirus E1A expression recruits primary rodent cells into proliferation but fails to transform them because of the induction programmed cell death (apoptosis). The adenovirus E1B 19,000-molecular-weight protein (19K protein), 55K protein, and human Bcl-2 each cause high-frequency transformation when coexpressed with by inhibiting apoptosis. Thus, requires deregulation growth be coupled suppression product p53 tumor suppressor gene induces apoptosis in transformed is required for E1A....
Big potassium (BK) ion channels have several spliced variants. One variant initially described within human glioma cells is the BK (gBK) channel. This isoform consists of 34 aa inserted into intracellular region basic PCR primers specific for this confirmed that cell lines and freshly resected surgical tissues from glioblastoma multiforme patients strongly expressed gBK mRNA. Normal brain tissue very weakly transcript. An Ab displayed protein in membrane, mitochondria, Golgi, endoplasmic...
Nonsteroidal anti-inflammatory drugs (NSAIDs) such as sulindac and indomethacin are a major cause of gastric erosions ulcers. Induction apoptosis by NSAIDs is an important mechanism involved. Understanding how affect genes that regulate useful for designing therapeutic or preventive strategies evaluating the efficacy safer being developed. We investigated whether growth arrest DNA damage-inducible 45α (GADD45α), stress signal response gene involved in regulation repair induction apoptosis,...
Portal hypertension (PHT) is associated with increased susceptibility of the gastric mucosa to injury by a variety factors, including nonsteroidal anti-inflammatory drugs (NSAIDs) that nonselectively inhibit both isoforms cyclooxygenase (COX-1 and -2). PHT also has excessive nitric oxide (NO) production contributes general injury. Using rat model PHT, we studied whether selective COX inhibition, which does not damage normal (normotensive) mucosa, sufficient cause and, if so, how NO involved....
Regulation of programmed cell death (apoptosis) has been known as a critical process in normal development and differentiation. More recently, apoptosis realized cellular response to growth deregulation that occurs during oncogenic transformation viral infection may indeed be defense mechanism for the elimination infected transformed cells. One best illustrations this activity is adenovirus expression transforming gene products.
Autophagy is a catabolic process by which cell degrades its intracellular materials to replenish itself. Induction of autophagy under various cellular stress stimuli can lead either survival or death via apoptotic and/or autophagic (nonapoptotic) pathways. The NSAID sulindac sulfide induces apoptosis in colon cancer cells. Here, we show that inhibition serum-deprived conditions resulted significant reductions sulfide-induced HT-29 In contrast, where serum available significantly increased We...
Estrogen receptors (ER) are present in various reproductive tissues as well other not considered classical targets for estrogen. A variety of alternatively spliced ER variants which co-exist with the wild-type receptor has also been described many tissues. We analyzed presence both and variant from normal human origin using semi-nested PCR direct automated sequence amplified products. demonstrate that contain a number estrogen receptor. Variants lacking exons 2, 4, 5, 7 detected