Showing papers in "Cell in 1990"

TL;DR: A model for the genetic basis of colorectal neoplasia that includes the following salient features is presented, which may be applicable to other common epithelial neoplasms, in which tumors of varying stage are more difficult to study.

TL;DR: Cet article synthese montre comment des recepteurs membranaires a activite tyrosine kinase peuvent etre impliques dans la transduction and notamment jouent le role de signal de the transduction.

TL;DR: It is demonstrated that the E6 proteins of the oncogenic HPVs that bind p53 stimulate the degradation of p53, which results in selective degradation of cellular proteins such as p53 with negative regulatory functions provides a novel mechanism of action for dominant-acting oncoproteins.

TL;DR: The predicted amino acid sequence of the nestin gene product shows that nestin defines a distinct sixth class of intermediate filament protein, extending a model in which transitions in intermediate filament gene expression reflect major steps in the pathway of neural differentiation.

TL;DR: In this paper, the authors have created soluble CD44-immunoglobulin fusion proteins and characterized their reactivity with tissue sections and lymph node high endothelial cells in primary culture.

TL;DR: It is suggested that follicular stem cells reside in the bulge region, instead of the lower bulb, which provides insights into hair cycle control and the possible involvement of hair follicle stem cells in skin carcinogenesis.

TL;DR: It is proposed that HLH proteins lacking a basic region may negatively regulate other HLHprotein through the formation of nonfunctional heterodimeric complexes.

TL;DR: The VCAM-1/VLA-4 ligand-receptor pair may play a major role in the recruitment of mononuclear leukocytes to inflammatory sites in vivo.

TL;DR: The genetic localization of this gene, its tissue-specific expression, and the function predicted from its sequence lead us to suggest that it represents the 11p13 Wilms' tumor gene.

TL;DR: It is proposed that the mutant versions of CFTR are recognized as abnormal and remain incompletely processed in the endoplasmic reticulum where they are subsequently degraded.

TL;DR: Coprecipitation experiments suggest direct AP-1-hormone receptor interaction, which also possibly explains the reverse experiment: overexpression of Fos or Jun inhibits the expression of hormone-dependent genes.

TL;DR: A modification of the polymerase chain reaction method is used to demonstrate that HIV-1 DNA synthesis is initiated in infected quiescent T cells at levels comparable with those of activated T cells.

TL;DR: Findings reveal a cross talk between two major signal transduction systems used to control gene transcription in response to extracellular stimuli, and a novel mechanism for transcriptional repression.

TL;DR: The Wnt-1 (int-1) proto-oncogene, which encodes a putative signaling molecule, is expressed exclusively in the developing central nervous system and adult testes and its normal role is in determination or subsequent development of a specific region of thecentral nervous system.

TL;DR: In vivo administration of SCF can reverse the macrocytic anemia and locally repair the mast cell deficiency of Sl/Sld mice and provide biological and physical evidence that SCF is a ligand for the c-kit receptor.

TL;DR: An A to G transition mutation at nucleotide pair 8344 in human mitochondrial DNA has been identified as the cause of MERRF, providing molecular confirmation that some forms of epilepsy are the result of deficiencies in mitochondrial energy production.

TL;DR: Yeast telomeres exert a position effect on the transcription of nearby genes, an effect that is under epigenetic control as demonstrated by phenotype and mRNA analyses.

TL;DR: A cloned gp130 could associate with a complex of IL-6 and solubleIL-6-R and transduce the growth signal when expressed in a murine IL-3-dependent cell line and confirmed that a gp130 is involved in the formation of high affinity IL- 6 binding sites.

TL;DR: Identification of two unique mutations within cardiac MHC genes in all individuals with FHC from two unrelated families demonstrates that defects in the cardiac M HC genes can cause this disease.

TL;DR: Evidence is presented that the glucocorticoid receptor (GR) and transcription factor Jun/AP-1 can reciprocally repress one another's transcriptional activation by a novel mechanism that is independent of DNA binding.

TL;DR: K, a hematopoietic growth factor obtained from conditioned medium of BALB/c 3T3 fibroblasts that stimulates the proliferation of mast cells and early erythroid progenitors, specifically binds to the c-kit receptor.

TL;DR: Northern analysis indicates a single species of mRNA for the TNF-R in a variety of cell types, therefore, the soluble TNF binding protein found in human serum is probably proteolytically derived from the T NF-R.

TL;DR: It is established that B27 plays a central role in the pathogenesis of the multi-organ system processes of the spondyloarthropathies and elucidation of the role of B27 should be facilitated by this transgenic model.

TL;DR: Findings provide evidence that members of the YPT1/SEC4 subfamily of GTP binding proteins are localized to specific exocytic and endocytic subcompartments in mammalian cells.

TL;DR: Evidence suggests that NF1 encodes a cytoplasmic GAP-like protein that may be involved in the control of cell growth by interacting with proteins such as the RAS gene product.

TL;DR: Within the hypervariable domain of p21K-ras(B), which is not palmitoylated, a novel plasma membrane targeting signal consisting of a polybasic domain that also acts in combination with the CAAX motif is identified.

TL;DR: Two distinct receptors for tumor necrosis factor (TNF) of 55 and 75 kd were expressed at low levels by various cells as discussed by the authors, and partial amino acid sequences were determined Short degenerate sense and antisense oligonucleotide primers encoding the N- and C-terminal ends of a peptide of 22 amino acid residues were used to amplify a 66 bp cDNA fragment from HL60 RNA by reverse transcriptase-polymerase chain reaction.

TL;DR: The TBR gene is established as the NF1 gene and a description of a major segment of the gene is provided, indicating base pair changes in the gene.

TL;DR: These findings strongly suggest that the TBR gene is the NF1 gene, and a number of cDNA clones from the translocation breakpoint region (TBR), one of which hybridizes to an approximately 11 kb mRNA.

TL;DR: These findings demonstrate that the failure of an effective antitumor immune response may be primarily due to a helper arm deficiency of the immune system rather than a paucity of tumor-specific cytotoxic effector cells and outline a novel strategy for augmenting tumor immunity.