Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

c-Myc inactivation by mutant Max alters growth and morphology of NCI-H-630 colon cancer cells.

Journal of cellular physiology - 1 Oct 1996

Borrè A, Cultraro C M, Segal S

Abstract excerpt

The myc gene family has been implicated in multiple cell processes including proliferation, differentiation, tumorigenesis, and apoptosis. For its cellular growth promoting function, Myc must heterodimerize with Max. To study the effect of Myc inactivation on the growth and differentiation properties of epithelial tumor cells, we transfected the H-630 human colon cancer cell line with bm-max, a mutant Max protein...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Cycle
Share to Cell Division
Share to DNA-Binding Proteins

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Gene Expression

Share to Gene Expression Regulation

Share to Mutation

Share to RNA, Messenger

Share to Transcription Factors

Source

Identifiers

PMID: 8841436
DOI: 10.1002/(SICI)1097-4652(199610)169:1<200::AID-JCP20>3.0.CO;2-F

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

c-Myc inactivation by mutant Max alters growth and morphology of NCI-H-630 colon cancer cells.PMID 8841436Read ↗

Transfected wild-type and mutant max regulate cell growth and differentiation of murine erythroleukemia cells.Semantic proximity Read ↗

Myc family oncoproteins function through a common pathway to transform normal cells in culture: cross-interference by Max and trans-acting dominant mutants.Semantic proximity Read ↗

Drosophila Myc is oncogenic in mammalian cells and plays a role in the diminutive phenotype.Semantic proximity Read ↗

Function of the c-Myc Oncogenic Transcription FactorSemantic proximity Read ↗

Opposite regulation of gene transcription and cell proliferation by c-Myc and Max.Semantic proximity Read ↗

Small-molecule inhibitors of c-Myc transcriptional factor suppress proliferation and induce apoptosis of promyelocytic leukemia cell via cell cycle arrestSemantic proximity Read ↗

Function of the c-Myc oncoprotein.Semantic proximity Read ↗

Mutational analysis of Max: role of basic, helix-loop-helix/leucine zipper domains in DNA binding, dimerization and regulation of Myc-mediated transcriptional activation.Semantic proximity Read ↗

Translocations involving c-myc and c-myc function.Semantic proximity Read ↗

Transactivation of the human p53 tumor suppressor gene by c-Myc/Max contributes to elevated mutant p53 expression in some tumors.Semantic proximity Read ↗

Myc and Max proteins possess distinct transcriptional activities.Semantic proximity Read ↗

In vivo quantification and perturbation of Myc-Max interactions and the impact on oncogenic potentialSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.