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PubMed2001

Expression of Id helix-loop-helix proteins in colorectal adenocarcinoma correlates with p53 expression and mitotic index.

Id helix-loop-helix (HLH) proteins function as regulators of cell growth and differentiation and when overexpressed can induce malignant transformation. In a series of 34 cases of primary human colorectal adenocarcinoma, immunoreactivity for Id1, Id2, and Id3 was found to be significantly elevated in tumor compared with normal mucosa (P = 0.001 for Id1 and Id2; P = 0.002 for Id3). No elevation of Id expression was observed in 17 cases of adenoma. Expression of Id1 and to a lesser extent of Id2 was correlated with mitotic index (P = 0.005 for Id1; P = 0.042 for Id2) in human adenocarcinomas, and expression of all three Id proteins was correlated with p53 immunoreactivity (a marker of mutational 'inactivation' of p53 function; P = 0.002 for Id1; P = 0.006 for Id2; P = 0.016 for Id3). In normal intestinal mucosa of p53-null mice and in spontaneous tumors arising in Min+/- mice, expression of all three Id proteins was also found to be up-regulated. Antisense oligonucleotide blockade of Id protein expression inhibited the proliferation of human adenocarcinoma cells. Enforced, ectopic expression of the E47 basic HLH (bHLH) protein in human adenocarcinoma cell lines efficiently sequestered endogenous Id proteins as Id-bHLH heterodimers, as shown by coimmunoprecipitation and subcellular colocalization studies. This led to growth arrest of the cells. Enforced overexpression of a mutant E47 protein, deficient in transactivation and DNA binding function, also partially inhibited cell growth. Taken together, these data imply that deregulated expression of Id proteins in colorectal adenocarcinoma arises at least in part as a consequence of loss of p53 function and contributes to the uncontrolled proliferation of tumor cells in colorectal cancer.

Adenocarcinoma↗
PubMed2006

[In vitro anti-tumor effect of CTL induced by HSP70-Id complex-modified dendritic cells].

OBJECTIVE: To prepare the tumor antigen peptide complex (HSP70-1d) of HSP70 and idiotype (Id) from SmIg ScFv fragment in patients with Chronic B cell leukemia (B-CLL), and to study the anti-tumor effect of cytotoxic T lymphocyte (CTL) induced by HSP70-Id complex-modified dendritic cell (DC) in vitro and explore their immune mechanism. METHODS: Purified HSP70 was combined into peptide complex (HSP70-Id) with the prepared Id-ScFv from B-CLL cells in vitro by using biochemical technique. The plastic-adherent monocytes from human peripheral blood were cultured and induced into DC with rhGM-CSF and rhIL-4 using cell culture and separation technique. The cultured DC were harvested and pulsed by HSP70-Id complex. DC morphology was observed under converted phase microscope and its phenotype was characterized by FCM on 8th day as well as their secreting cytokines were measured. Host lymphocytes were stimulated by DC loaded with HSP70-Id complex and co-cultured in the medium containing IL-2. The activation and proliferation of lymphocytes were examined by MTr test, which was also used to assay cytotoxicity of CTL elicited by modified DC to Daudi, K562 and HepG2 tumor cells, and FCM analyzed the changes of T lymphocyte subsets. RESULTS: Mature DCs were obtained successfully, showing typical morphology and phenotypic properties, the expression ratio of cellular surface molecules, CD1a was 20% - 30%, CD83 was more than 72% , both CD86 and HLA-DR over-expressed obviously in the complex-loaded DC group secreting cytokines of Thl type, IL-12 and TNF-alpha. The culturing lymphocytes that were activated by modified DC could more effectively and specifically kill Daudi (71. 24%), but not K562 and HepG2 tumor cells. Results of FCM assay demonstrated that percentage of CD4+ and CD8+ T lymphocytes cocultured with complex-modified DC increased notably to 56.51% and 70.21%, respectively. CD4+ T/ CD8+ T proportion was changed from 1.49 to 0.81. The dose of peptide would be reduced to 1/50 if specific CTL induced by complex-modified DC instead of directly by peptide complex. CONCLUSION: DCs modified by HSP70-Id complex exhibit powerful biological activities, and could induce CTL to specific cytotoxicity against carcinoma cells. It might be produced by cooperation of CD4+ T, CD8+ T lymphocytes and DC. The results also suggested that DC modified by HSP70-Id complex can present antigen and induce CTL with high efficacy and specificity.

Cell Line, Tumor↗
PubMed1986

The lymphokine "inhibitor of DNA synthesis" (IDS) suppresses human T lymphocyte proliferation by an interleukin-2-independent mechanism.

IDS is a soluble glycoprotein product of activated T cells that inhibits lymphocyte proliferation induced by antigens and by lectin mitogens. This immunosuppressive lymphokine has been distinguished from lymphotoxin, Proliferation Inhibitory Factor, Colony Inhibitory Factor, Macrophage Inhibitory Factor, and interferon. Using IDS partially purified by isoelectric focusing from culture supernatants of concanavalin A-stimulated human peripheral blood mononuclear cells (PBMC), we investigated IDS inhibition of T cell proliferation with respect to the interleukin pathway. At concentrations that produced 75-90% suppression of proliferation in PHA-stimulated PBMC cultures, IDS caused no decrease in interleukin 2 (IL2) production (determined by bioassay) or in IL2 receptor expression (determined with anti-Tac antibody). Moreover, adding exogenous IL2 to IDS-inhibited cultures failed to restore proliferation. IDS inhibited growth of several IL2-dependent and IL2-independent cell lines, and suppressed proliferation of PBMC induced by the phorbol ester TPA (12-0-tetradecanoyl-13-phorbol acetate) or by the calcium ionophore A23187, thus distinguishing its mechanism of action from that of cyclosporin A, dexamethasone, OKT11A antibody, and other inhibitors. These data extend earlier findings that IDS acts late in G1 phase of the cell cycle, and provide evidence that IDS inhibits T cell proliferation through an IL2-independent mechanism.

Animals↗
PubMed1996

IDS gene-pseudogene exchange responsible for an intragenic deletion in a Hunter patient.

Hunter disease or mucopolysaccharidosis type II is an X-linked disease caused by the deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). The IDS gene (24 kb) contains nine exons and has been completely sequenced. A pseudogene (IDS-2 locus) distal to the functional IDS gene has recently been identified. This work reports the characterization of IDS gene alterations in two severely affected patients. Patient 1 has a partial deletion that removes exons I to VI and extends about 200 kb upstream of the IDS gene. Patient 2 has an internal deletion of exons IV, V, VI, and VII, which results from an IDS gene-pseudogene exchange between highly homologous regions. In the rearranged gene, the junction intron contains pseudogene intron 3- and intron 7-related sequences. An interchromosomal recombination is probably the cause of this rearranged X chromosome.

Gene Rearrangement↗
PubMed1994

Regulation of G1 progression by E2A and Id helix-loop-helix proteins.

In NIH3T3 fibroblasts, the ubiquitous helix-loop-helix (HLH) protein E2A (E12/E47) and the myogenic HLH proteins MyoD, MRF4 and myogenin are growth-inhibitory, while two ubiquitous Id proteins lacking the basic region are not. The dimerization domain mediates inhibition. However, in addition to the HLH region, E2A contains two inhibitory regions over-lapping with the main transcriptional activation domains. The growth-suppressive activity of the intact E47 as well as MyoD was counteracted by the Id proteins. When E47 lacking the HLH domain was overexpressed, Id could no longer reverse growth inhibition. By increasing the amount of E47 with an inducible system or neutralizing the endogenous Id with microinjected anti-Id antibodies, withdrawal from the cell cycle occurred within hours before the G1-S transition point. The combined results suggest that the Id proteins are required for G1 progression. The antagonism between the E2A and Id proteins further suggests that both are involved in regulatory events prior to or near the restriction point in the G1 phase of the cell cycle.

3T3 Cells↗
PubMed1999

Effects of wild-type and mutated p53 and Id proteins on the induction of apoptosis by adenovirus E1A, c-Myc, Bax, and Nip3 in p53 null mouse cerebellum cells.

The sensitivities of apoptosis induced by E1A, c-Myc, Bax, and Nip3 to wild-type (wt) and mutated p53 and Id proteins were analyzed by transient transfection followed by flow cytometry with p53 null mouse cerebellum cell lines W7 and M13 that express wt and mutated p53 in response to dexamethasone, respectively. Apoptosis induced by c-Myc was stimulated weakly by wt p53, strongly by Ids, but suppressed completely by mutated p53 irrespective of coexpression with Ids, while apoptosis induced by E1A was suppressed by mutated p53 but stimulated when coexpressed with Ids. Apoptosis induced by Bax was little affected by wt and mutated p53, but inhibited by Ids, while apoptosis induced by Nip3 was inhibited by both wt and mutated p53 and inhibition was stimulated by Ids. Caspase-1 was activated only by Bax significantly when coexpressed with mutated p53 but not with wt p53. These results indicate that the apoptotic processes elicited by these inducers are different and differently affected by wt and mutated p53 and by Ids.

Adenovirus E1A Proteins↗
PubMed1978

The effects of a new benzodiazepine derivative, ID-540, on the averaged photopalpebral reflex in man.

The effects of 7-chloro-5-(2-fluorophenyl)-1-methyl-1 H, 1.4-benzodiazepin-2(3H)-one (ID-540), a recently introduced benzodiazepine derivative, on the averaged photopalpebral reflex (PPR), subjective symptoms, and serum levels of ID-540 and its principal metabolite, N-desmethyl-ID-540, following an oral dose of 0.5 mg or placebo were investigated in six male Japanese students in a double-blind, crossover design. The peak latencies of PPR showed a statistically significant prolongation, with maximum level at 3 h after administration, which recovered to the initial level within 4 h. The amplitude of PPR failed to show a definite response to the drug. The serum concentration of ID-540 reached a peak level 2-3 h after administration, and then decreased at 4 h. N-Desmethyl-ID-540 exhibited a slow- gradual rise in serum. The latencies of PPR were positively correlated with the serum level of ID-540 but not with the N-desmethyl-ID-540. It is concluded that the PPR test may be a useful method for predicting the clinical effects of psychotropic drugs.

Adult↗
PubMed1996

Attenuated function of a variant form of the helix-loop-helix protein, Id-3, generated by an alternative splicing mechanism.

The Id family of helix-loop-helix proteins function as negative regulators of DNA binding, basic helix-loop-helix proteins in the regulation of cell growth and differentiation. We report here on the identification of a 17 kDa variant of the 14 kDa Id-3 protein termed Id-3L (long version) which possesses a unique 60 amino acid carboxy-terminus generated by read through of a 'coding intron' and alternative splicing. Northern analysis revealed expression of a minor 1.1 kb Id-3L transcript together with the predominant 0.95 kb Id-3 transcript in the majority of adult human tissues analysed. The variant Id-3L protein is functionally distinguishable from conventional Id-3 since in in vitro DNA mobility shift assays, it was greatly impaired in its ability to abrogate binding of the basic helix-loop-helix protein, E47, to an E box recognition sequence.

Adult↗
PubMed2005

Identification and expression profile of the ID gene family in the rainbow trout (Oncorhynchus mykiss).

ID proteins are negative regulators of basic helix-loop-helix transcription factors governing growth and development in mammals. However, little is known about the ID gene function and expression in fish. We report the identification and characterization of two new rainbow trout ID genes (ID1D and ID2B) and extend our expression analyses of two previously identified ID genes (ID1A and ID2A). Phylogenetic analyses indicate an evolutionary relationship between ID1A and ID1D and between ID1B and ID1C, suggesting a mechanism of divergence throughout salmonid evolution. To access the expression of these genes in adult and developing fish, we measured the relative transcript abundance of four ID1 and two ID2 genes by real-time PCR. ID1 transcripts were expressed in a variety of tissues and the ID1 paralogues showed similar patterns of expression, whereas the ID2 paralogues were differentially expressed. To access the role of the ID genes during embryonic development, gene expression was measured at early (day 0 and day 2), mid (day 9 and day 18) and late (day 30 and day 50) embryonic development. ID1A and ID1D expression remained unchanged throughout embryonic development, while ID1B and ID1C were lowest during early, highest at mid, and decreased during late embryonic development. The ID2 transcripts revealed the highest expression in unfertilized eggs and day 2 embryos, and remained low throughout the remainder of embryonic development. The sequence analyses and gene expression patterns implicate gene and genome duplication in rainbow trout ID gene evolution and suggest an extensive role for the IDs in rainbow trout growth and development.

Animals↗
PubMed2006

Helicobacter pylori regulates the expression of inhibitors of DNA binding (Id) proteins by gastric epithelial cells.

Id transcription factors control proliferation, differentiation and apoptosis by inhibiting the DNA binding of basic helix-loop-helix transcription factors. Increased expression of Id proteins promotes proliferation, inhibits differentiation, and is associated with intestinal tumorigenesis. We aimed to determine how Helicobacter pylori may alter the expression of Id proteins by gastric epithelial cells: it was hypothesised that H. pylori, a known carcinogen, would result in increased expression of one or more Id family members. In vitro and in vivo models of infection were employed, including treatment of AGS gastric epithelial cells with wild-type H. pylori strains, 60190 and SS1, and Mongolian gerbils infected with H. pylori SS1. A small cohort of human gastric mucosal biopsies was also examined. Treatment of AGS cells with H. pylori resulted in down-regulation of Id1 and Id3. Unexpectedly, expression of the main target of Id proteins, the basic helix-loop-helix transcription factor E2A, was also suppressed, with an associated decrease in E-box binding activity. In contrast, H. pylori induced the expression of the CDK inhibitor p21(WAF-1/cip1), and the homeobox transcription factor, Cdx2, an early marker of intestinal metaplasia of the stomach epithelium. Gastric epithelium from H. pylori-infected gerbils demonstrated similar changes, with decreased Id2, Id3 and E2A, and elevated p21(WAF-1/cip1) expression. In human gastric epithelium also, H. pylori infection was associated with reduced Id and E2A expression. In conclusion, H. pylori alters the expression of Id proteins, in vitro and in vivo; it is hypothesised that these changes contribute to H. pylori-associated pathologies.

Adolescent↗
PubMed2003

Cloning and characterization of Xenopus Id4 reveals differing roles for Id genes.

We have identified Xenopus Id4, a member of the Id (inhibitor of differentiation/DNA binding) class of helix-loop-helix proteins. Id factors dimerize with general bHLH factors, preventing their interaction with tissue-specific bHLH factors, to inhibit premature differentiation. The presence of several Id proteins could reflect simple redundancy in function, or more interestingly, might suggest different activities for these proteins. During embryonic development, Xenopus Id4 is expressed in a number of neural tissues, including Rohon-Beard neurons, olfactory placode, eye primordia, and the trigeminal ganglia. It is also expressed in other organs, such as the pronephros and liver primordium. As embryogenesis progresses, it is expressed in the migrating melanocytes and lateral line structures. We compare the expression of Id4 mRNA with that of Id2 and Id3 and find that the Id genes are expressed in complementary patterns during neurogenesis, myogenesis, kidney development, in the tailbud, and in the migrating neural crest. To examine the regulation of Id gene expression during Xenopus neural development, we show that expression of Id3 and Id4 can be induced by overexpression of BMP4 in the whole embryo and in ectodermal explants. Expression of Id2, Id3, and Id4 in these explants is unaffected by the expression of FGF-8 or a dominant-negative Ras (N17ras), suggesting that Id genes are not regulated by the FGF signaling pathway in naive ectoderm. We also show that Notch signaling can activate Id2 and Id3 expression in the whole embryo. In contrast, Id4 expression in the Rohon-Beard cells is inhibited by activated Notch and increased by a dominant-negative Delta. This may reflect an increase in Rohon-Beard cells in response to inhibition of Notch signaling rather than transcriptional regulation of Id4. Finally, to compare the activities of Id2, Id3, and Id4, we use animal cap explants and in vivo overexpression to show that Id proteins can differentially inhibit the activities of neurogenin and neuroD, both neurogenic bHLH molecules and MyoD, a myogenic bHLH protein. Id4 is able to inhibit the activity all these bHLH molecules, Id2 inhibits MyoD and neuroD, while Id3 blocks only neuroD activity in our assays.

Amino Acid Sequence↗
PubMedDate not supplied

Examination of the short form of the Inventory of Drinking Situations (IDS-42) in a young adult university student sample.

The 42-item version of the Inventory of Drinking Situations (IDS-42) assesses relative frequency of drinking behavior across eight categories of drinking situations and was originally developed as a method for identifying high-risk situations in alcoholic samples. This study was designed to examine the psychometric properties of the IDS-42 in a sample of university students in order to assess its suitability as an assessment tool in the non-clinical population. Three hundred and ninety-six students (111 M, 283 F, 2 with missing gender data) completed the IDS-42 and a well established measure of drinking motives, the Drinking Motives Questionnaire (DMQ). Confirmatory factor analysis of the IDS-42 established a hierarchical factor structure with eight lower-order factors and three higher-order factors of negatively-reinforcing situations, positively-reinforcing situations, and temptation situations. The eight lower-order IDS-42 factors demonstrated moderate to high internal consistency and excellent concurrent validity with conceptually-similar DMQ subscale scores. Non-parametric analyses revealed that male students reported a higher drinking frequency overall as compared to female students, particularly in IDS-42 situations involving Social Pressure to Drink, Pleasant Times with Others, Testing Personal Control, and Urges and Temptations. Across the entire sample of university student drinkers, a higher drinking frequency was reported in positively-reinforcing situations as compared to negatively-reinforcing situations and temptation situations, as predicted. Results suggest the IDS-42 possesses good psychometric properties and support its utility as a tool in identifying situation-specific antecedents to drinking among university students.

Adolescent↗
PubMed2004

Id proteins in neural cancer.

Id proteins are general inhibitors of differentiation and positive regulators of proliferation in the nervous system. The role of Id is especially evident in neural development, a period during which Id proteins prevent premature differentiation and terminal cell cycle arrest. These activities have been related to the recognized ability of Id proteins to antagonize basic helix loop helix transcription factors and proteins of the Retinoblastoma tumor suppressor family. In recent experiments, it was shown that Id proteins-normally low or absent in post-natal tissues-are abnormally expressed by tumor and endothelial cells of neoplasms derived from the central nervous system and peripheral nervous system. In these tumors, deregulated Id activity has been associated with relentless proliferation, loss of differentiation and neo-angiogenesis, all key features of neural tumor progression. Future work will be required to fully elucidate the molecular networks engaged by Id proteins to contribute to the essential hallmarks of neural cancer.

Animals↗
PubMed2002

Down-regulation of Id-1 expression is associated with TGF beta 1-induced growth arrest in prostate epithelial cells.

Transforming growth factor beta1 (TGF beta 1) plays important roles in the regulation of cell growth and differentiation in both normal and malignant prostate epithelial cells. Although certain pathways have been suggested, the mechanisms responsible for the action of TGF beta 1 are not well understood. In the present study, using a human papilloma virus 16 E6/E7 immortalized prostate epithelial cell line, HPr-1, we report that TGF beta 1 was able to suppress the expression of Id-1, a helix-loop-helix (HLH) protein, which plays important roles in the inhibition of cell differentiation and growth arrest. In addition, a decrease at both Id-1 mRNA and protein expression levels was associated with TGF beta 1-induced growth arrest and differentiation, indicating that Id-1 may be involved in TGF beta 1 signaling pathway. The fact that up-regulation of p21(WAF1), one of the downstream effectors of Id-1, was observed after exposure to TGF beta 1 further indicates the involvement of Id-1 in the TGF beta 1-induced growth arrest in HPr-1 cells. However, increased expression of p27(KIP1) was also observed in the TGF beta 1-treated cells, suggesting that in addition to down-regulation of Id-1, other factors may be involved in the TGF beta 1-induced cell growth arrest and differentiation in prostate epithelial cells. Our results provide evidence for the first time that TGF beta 1 may be one of the upstream regulators of Id-1.

Blotting, Western↗
PubMed2003

Role for Id-1 in immunobiology of normal keratinocytes and in basal cell carcinoma.

It has been established that Id proteins can block the basic helix-loop-helix (HLH) transcription factors, thereby impacting the onset of senescence in keratinocytes, as well as influencing tumorigenesis involving squamous cell carcinomas. However, the ability of Id-1 to influence the immunologic response of epithelial cells to cytokines implicated in cutaneous oncology such as gamma interferon (IFN-gamma) has not been determined. Using a whole population of human keratinocytes infected with a retrovirus to induce over-expression of Id-1, the influence on early differentiation of rapidly proliferating keratinocytes was assessed, as was the response to IFN-gamma. While induction of involucrin, a marker of early differentiation, was not altered in Id-1 overexpressing keratinocytes, the IFN-gamma mediated increase in intercellular adhesion molecule-1 (ICAM-1) and HLA-DR was reduced. No change in constitutive or inducible levels of MHC class I antigen, CD95 (Fas antigen) or LFA-3 (CD58) was observed in this system. Immunostaining and Western blot analysis revealed over-expression of Id-1 in basal cell carcinomas (BCCs). These tumors not only strongly and diffusely expressed Id-1, but were also characterized by reduced ICAM-1 and HLA-DR expression. Thus, dysregulated Id-1 may not only contribute to delaying the senescence program in keratinocytes, it may also contribute to the escape of the relatively undifferentiated tumor cells in BCC from immune surveillance.

Antineoplastic Agents↗
PubMed2001

Id proteins at the cross-road of development and cancer.

A large body of evidence has been accumulated that demonstrates dominant effects of Id proteins on different aspects of cellular growth. Generally, constitutive expression of Id not only blocks cell differentiation but also drives proliferation. In some settings, it is sufficient to render cells immortal or induce oncogenic transformation. The participation of Id proteins in advanced human malignancy, where they are frequently deregulated, has been dramatically bolstered by the recent discovery that Id exert pivotal contributions to many of the essential alterations that collectively dictate malignant growth. Relentless proliferation associated with self-sufficiency in growth signals and insensitivity to growth inhibitory signals, sustained neoangiogenesis, tissue invasiveness and migration capabilities of tumor cells all share dependency on the unlimited availability of Id proteins. It is remarkable that many of these features recapitulate those physiologically propelled by Id proteins to support normal development. We propose that the participation of Id in multiple fundamental traits of cancer may be the basis for unprecedented therapeutic opportunities.

Animals↗
PubMed2003

Glasgow Anxiety Scale for people with an Intellectual Disability (GAS-ID): development and psychometric properties of a new measure for use with people with mild intellectual disability.

BACKGROUND: Self-rating scales are widely used in general adult practice; however, there is no reliable and valid method for assessing state anxiety in people with intellectual disability (ID). The present study describes the development and psychometric evaluation of a new scale, the Glasgow Anxiety Scale for People with an Intellectual Disability (GAS-ID). METHODS: First, an item pool was generated from focus groups, a review of the literature and clinician feedback. Secondly, a draft scale was administered to 19 anxious and 16 non-anxious people with ID for further validation and appraisal of reliability. Thirdly, the scale was completed by 19 anxious, non-ID people for cross-validation with the Beck Anxiety Inventory (BAI). Finally, physiological concomitants were validated by pulse-oximetry. RESULTS: The 27-item GAS-ID discriminated anxious from non-anxious participants, had good test-retest reliability (r = 0.95) and internal consistency (alpha = 0.96), and was reasonably correlated with the BAI (rho = 0.75). The correlation between the physiological subscale of the GAS-ID and changes in pulse rate was moderately significant (rho = 0.52). CONCLUSIONS: This preliminary study suggests that the GAS-ID offers a psychometrically robust and practical (5-10 min) approach to the appraisal of anxiety in this population.

Adult↗
PubMed2001

Molecular cloning and characterization of a zinc finger protein involved in Id-1-stimulated mammary epithelial cell growth.

Id proteins are dominant negative regulators of basic helix-loop-helix transcription factors. Previous work in our laboratory has shown that constitutive expression of Id-1 in SCp2 mouse mammary epithelial cells inhibits their differentiation and induces proliferation, invasion, and migration. Id-1 expression also correlates with the invasive and aggressive potential of human breast cancer cells. However, little is known about Id-1 target genes that are important for regulating normal and transformed breast epithelial cell phenotypes. Now we report the cloning of a novel zinc finger protein, Zfp289, using degenerate primers to specifically amplify cDNAs from Id-1-transfected SCp2 cells. Zfp289 has homology with a yeast zinc finger protein, the GTPase-activating protein Gcs-1, which was initially identified as a gene required for the re-entry of cells into the cell cycle after stationary phase growth. Zfp289 mRNA expression pattern correlates with Id-1 expression in SCp2 mammary epithelial cells under various experimental conditions as well as in the mouse mammary gland at different stages of development. It is predominantly present in the cytoplasm of the cells as evident from green fluorescent protein fusion protein localization. SCp2 mammary epithelial cells with constitutive expression of Zfp289 have a higher S-phase index, compared with control cells, when cultured in a serum-free medium. We conclude that the novel zinc finger protein Zfp289, which may represent the mammalian homologue of Gcs-1, is potentially an important mediator of the Id-1-induced proliferation pathway in mammary epithelial cells.

Amino Acid Sequence↗