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Biomedical subjects

G E Gallick

Publications and source records attributed to G E Gallick.

62 records · Page 4Linked to original sources
PubMed1983

A group of temperature-sensitive mutants of Moloney leukemia virus which is defective in cleavage of env precursor polypeptide in infected cells also induces hind-limb paralysis in newborn CFW/D mice.

A group of temperature sensitive mutants of Moloney murine leukemia virus (MoMuLV) designated as ts1, ts7, and ts11 rapidly and invariably induce hind-limb paralysis ranging from 28 to 52 days postinjection of neonatal CFW/D mice. These temperature-sensitive mutants are defective in the processing of the precursor of the env protein, gPr80env in infected cells, resulting in the accumulation of gPr80env in the infected cell and production of virions with reduced amounts of gp70, p15E, and p12E when compared to that of the wild-type virion. In contrast, two nonparalytogenic ts mutants, ts3 and ts10, like the wild-type virus, show normal processing of gPr80env in infected cells and production of virions with a similar amount of env proteins to that of the wild-type virion.

Animals↗
PubMed1983

P85gag-mos encoded by ts110 Moloney murine sarcoma virus: rapid at the restrictive temperature.

The stability of P85gag-mos, encoded by ts110 Moloney murine sarcoma virus, was studied. P85gag-mos was found to turn over more rapidly at 39 degrees C than 33 degrees C in two different cell lines. One of these is a non-producer cell clone (6m2) which appears only to express P85 at 33 degrees C. The other cell line (206-2IC) produces P85gag-mos at both 33 degrees C and 39 degrees C, although in lower amounts at the higher temperature. Both cell lines exhibit the normal morphological phenotype following a shift to the restrictive temperature. These data suggest that the presence of P85gag-mos alone is insufficient to cause transformation, and that some function(s) associated with the molecule may be heat-labile.

Animals↗
PubMed1983

P85: a gag-mos polyprotein encoded by ts110 Moloney murine sarcoma virus.

Antibody to a synthetic peptide (anti-C3 serum) with the predicted sequence of the C terminus of the Moloney murine sarcoma virus (strain 124) v-mos gene was used in immunoprecipitation experiments with cytoplasmic extracts of a clone of NRK cells infected with ts110 Moloney murine sarcoma virus, termed 6m2 cells. ts110 Moloney murine sarcoma virus codes for two viral proteins of 85,000 and 58,000 M(r), termed P85 and P58, respectively, in nonproducer 6m2 cells maintained at 33 degrees C. Anti-C3 serum specifically recognized [(3)H]leucine-labeled P85, but not P58, from infected cells maintained at 33 degrees C, whereas antiserum prepared against murine leukemia virus p12 recognized both proteins. Normal serum and anti-C3 serum pretreated with excess C3 peptide did not precipitate P85. Immunoprecipitation experiments after metabolic labeling of 6m2 cells with (32)P(i) showed that P85 is phosphorylated. Both anti-C3 and anti-p12 sera specifically detected (32)P-labeled P85. Cell-free translation of ts110 murine sarcoma virus/murine lukemia virus RNA produces P85, P58, and helper virus protein Pr63(gag). Anti-C3 serum specifically precipitated P85 but neither P58 nor Pr63(gag). We conclude from these studies that P85 is a product of both the gag and mos genes of ts110 murine sarcoma virus, and, therefore, it is referred to as P85(gag-mos). We have not detected any other v-mos gene product in ts110-infected cells.

Animals↗
PubMed1980

A fast replica plating technique for the isolation of post-integration mutants of the Moloney strain of murine leukaemia virus.

Seven temperature-sensitive (ts) mutants of Moloney murine leukaemia virus (Mo-MuLV) were isolated using a rapid, non-selective replica plating technique designed to select for post-integration mutants. Thymus-bone marrow (TB) cells, infected with mutagenized virus, were cloned and incubated at the non-permissive temperature (39 degrees C) for 10 days. The resulting colonies were screened for production of virus by replica plating supernatant from the "master" tray on to a second tray pre-seeded with fu-1 (a cell line derived from L8 myoblasts) indicator cells. The "master" tray was shifted to the permissive temperature (34 degrees C) for 48 h, then re-screened for virus production. Any colony on the "master" tray which produced syncytia-inducing virus at 34 degrees C but not at 39 degrees C was potentially producing a ts mutant. Preliminary characterization by shift-down experiments and scanning electron microscopy of three of the ts mutants isolated by this technique revealed a mutant blocked before budding, one blocked at an early stage in the budding process and one with a defect after release of the virus.

Animals↗
PubMed1978

Preliminary characterization of a temperature-sensitive mutant of Moloney murine leukemia virus that produces particles at the restrictive temperature.

The isolation and preliminary characterization of a new temperature-sensitive mutant of Moloney murine leukemia virus, designated ts7, are reported. The infectivity of ts7, determined by a focus-forming unit assay, was reduced at least 100-fold when the virus was assayed at the nonpermissive temperature (39 degrees C) as compared with assay at the permissive temperature (34 degrees C). However, several lines of evidence indicated that the diminution of ts7 titer at 39 degrees C is not due to its inability to form virus particles at that temperature. The supernatant from ts7-infected cells grown at 39 degrees C showed significant infectivity when assayed at 34 degrees C; only small reductions in reverse transcriptase activity and fusion ability were observed when compared with supernatant from 34 degrees C ts7-infected cultures. That particles are produced at the nonpermissive temperature was confirmed by transmission electron microscopy of the supernatant from ts7-infected cells at 39 degrees C and by transmission electron microscope observations of mature particles trapped in the intercellular spaces of pelleted thin cell section. A possible explanation for the productivity at 39 degrees C of particles that are infectious at 34 degrees C but not at 39 degrees C is that the virus is heat labile at the nonpermissive temperature. Consistent with this hypothesis is the extreme heat lability of virus harvested at 34 degrees C. Such virus, when incubated at 39 degrees C, has a half-life one-sixth that of identical virus incubated at 34 degrees C, or that of wild-type virus at either temperature.

Cell Fusion↗
PubMedDate not supplied

Overexpression of focal adhesion kinase (p125FAK) in human colorectal carcinoma liver metastases: independence from c-src or c-yes activation.

BACKGROUND: p125FAK, pp60C-src, and pp62c-yes are protein tyrosine kinases that function in signaling pathways regulating cell adhesion, migration, and growth. The expression and tyrosine kinase activities of pp60c-src and pp62c-yes, and the expression of p125FAK are increased in colorectal tumor metastases relative to normal mucosa. This study investigates whether differences in the activation of pp60c-src and pp62c-yes in colorectal liver metastases correlated with differences in p125FAK expression and whether prognostic significance could be demonstrated from the extent of expression of p125FAK in metastases. METHODS: Activities of pp60c-src and pp62c-yes were measured in the immune complex kinase assay. Relative levels of p125FAK, pp60c-src, and pp62c-yes were determined by immunoblotting. RESULTS: p125FAK was overexpressed in 29 of 30 colorectal cancer liver metastases (range of two-to 195-fold increase compared with normal mucosa). The degree of overexpression of p125FAK was not a significant prognostic factor in survival. A differential activation of pp60c-src and pp62c-yes in colorectal carcinoma liver metastases was observed. However, overexpression of p125FAK was observed in metastases with either pp60c-src or pp62c-yes activated in colorectal carcinoma liver metastases. CONCLUSIONS: p125FAK overexpression appears to be a marker present in colorectal cancer cells with a metastatic phenotype. Furthermore, p125FAK overexpression is independent of pp60c-src or pp62c-yes activation in human colorectal carcinoma liver metastases.

Biomarkers, Tumor↗
PubMedDate not supplied

The biology of colorectal carcinoma.

Rapid progress in understanding the biology of colorectal carcinoma has occurred in the last decade. During this time, the importance of tumor suppressor genes has been delineated. Mutations in proto-oncogenes, and some of the genetic and epigenetic defects that occur during neoplastic transformation, have been characterized. The very recent identification of a technology that detects some mutations in genes by analyzing fecal specimens offers the real prospect of effective, low-cost screening of large segments of the population at risk for the development of large bowel cancer. A better understanding of the mechanisms involved in metastasis is slowly leading to better methods of prognostication for patients with carcinoma of the colon or rectum. This is important because a better biologic identification of patients at high risk for subsequent metastasis will help determine which patients should receive adjuvant therapy. Further, the development of new approaches to inhibit various aspects of the cascade of events necessary to produce metastasis, notably the inhibition of neovascularization, suggests the real possibility that established metastases may be treated by relatively nontoxic medical therapies. As a result, further knowledge of the biology of colorectal cancer will translate into strategies that will continue to improve the control of this prevalent carcinoma.

Adenoma↗