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Biomedical subjects

S Eisenberg

Publications and source records attributed to S Eisenberg.

At least 19 recordsLinked to original sources
PubMed2001

A single nucleotide polymorphism in the RAD51 gene modifies cancer risk in BRCA2 but not BRCA1 carriers.

BRCA1 and BRCA2 carriers are at increased risk for both breast and ovarian cancer, but estimates of lifetime risk vary widely, suggesting their penetrance is modified by other genetic and/or environmental factors. The BRCA1 and BRCA2 proteins function in DNA repair in conjunction with RAD51. A preliminary report suggested that a single nucleotide polymorphism in the 5' untranslated region of RAD51 (135C/G) increases breast cancer risk in BRCA1 and BRCA2 carriers. To investigate this effect we studied 257 female Ashkenazi Jewish carriers of one of the common BRCA1 (185delAG, 5382insC) or BRCA2 (6174delT) mutations. Of this group, 164 were affected with breast and/or ovarian cancer and 93 were unaffected. RAD51 genotyping was performed on all subjects. Among BRCA1 carriers, RAD51-135C frequency was similar in healthy and affected women [6.1% (3 of 49) and 9.9% (12 of 121), respectively], and RAD-135C did not influence age of cancer diagnosis [Hazard ratio (HR) = 1.18 for disease in RAD51-135C heterozygotes, not significant]. However, in BRCA2 carriers, RAD51-135C heterozygote frequency in affected women was 17.4% (8 of 46) compared with 4.9% (2 of 41) in unaffected women (P = 0.07). Survival analysis in BRCA2 carriers showed RAD51-135C increased risk of breast and/or ovarian cancer with an HR of 4.0 [95% confidence interval 1.6-9.8, P = 0.003]. This effect was largely due to increased breast cancer risk with an HR of 3.46 (95% confidence interval 1.3-9.2, P = 0.01) for breast cancer in BRCA2 carriers who were RAD51-135C heterozygotes. RAD51 status did not affect ovarian cancer risk. These results show RAD51-135C is a clinically significant modifier of BRCA2 penetrance, specifically in raising breast cancer risk at younger ages.

Adult↗
PubMed2000

Expression of the familial Mediterranean fever gene and activity of the C5a inhibitor in human primary fibroblast cultures.

Familial Mediterranean fever (FMF) is an inherited disease whose manifestations are acute but reversible attacks of sterile inflammation affecting synovial and serosal spaces. The FMF gene (MEFV) was recently cloned, and it codes for a protein (pyrin/marenostrin) homologous to known nuclear factors. We previously reported the deficient activity of a C5a/interleukin (IL)-8 inhibitor, a physiologic regulator of inflammatory processes, in FMF serosal and synovial fluids. We now describe the concomitant expression of MEFV and C5a/IL-8-inhibitor activity in primary cultures of human fibroblasts. Fibroblasts grown from synovial and peritoneal tissues displayed C5a/IL-8-inhibitor activity that could be further induced with phorbol myristate acetate (PMA) and IL-1 beta. Very low levels of chemotactic inhibitor were evident in skin fibroblast cultures or in peritoneal and skin fibroblasts obtained from FMF patients. MEFV was expressed in peritoneal and skin fibroblasts at a lower level than in neutrophils and could be further induced by PMA and IL-1 beta. In the FMF cultures, the MEFV transcript carried the M694V mutation, consistent with the genetic defect found in patients with this disease. MEFV was also expressed in other cell lines that do not produce C5a/IL-8 inhibitor. These findings suggest that human primary fibroblast cultures express MEFV and produce C5a/IL-8-inhibitor activity. The interrelationship between pyrin, the MEFV product, and the C5a/IL-8 inhibitor requires further investigation. (Blood. 2000;96:727-731)

Cells, Cultured↗
PubMed2000

BRCA1 and BRCA2 mutation carriers as potential candidates for chemoprevention trials.

The identification of cancer susceptibility genes offers new avenues for selecting high-risk individuals as subjects for chemoprevention trials. Because carriers of predisposing mutations are at high risk, they are more likely to enroll and comply with chemoprevention trials, and meaningful results can be achieved with smaller numbers of participants and shorter periods of follow-up. Such studies have immediate benefits for carriers themselves, but they are also likely to result in effective chemopreventive strategies for the general population. In this review, we discuss BRCA1 and BRCA2 carriers as potential candidates for breast and ovarian cancer chemoprevention trials. The existence of a large population with a high frequency of easily identifiable BRCA1/2 mutations can provide ample opportunity for such studies. However, the possibility that tumor characteristics and hormonal profile of BRCA1/BRCA2 related cancers are not completely equivalent to cancers in the general population should be borne in mind.

Anticarcinogenic Agents↗
PubMed1998

Diagnosis of familial Mediterranean fever by a molecular genetics method.

BACKGROUND: Familial Mediterranean fever is a recessively inherited disorder characterized by episodes of fever with abdominal pain, pleurisy, or arthritis. The familial Mediterranean fever gene, designated MEFV, was recently cloned, and at least three missense mutations (M6801, M694V, and V726A) that account for a large percentage of patients with this disease were identified. OBJECTIVE: To establish a diagnostic test for familial Mediterranean fever. DESIGN: Cross-sectional study of a convenience sample of patients attending familial Mediterranean fever clinics. SETTING: Tertiary referral hospitals. PATIENTS: 107 patients with familial Mediterranean fever, their family members, and controls. MEASUREMENTS: Mutations in the 107 samples were assessed by amplifying genomic DNA with use of primers that selectively amplify the normal or altered DNA sequence of the 3 MEFV mutations (amplification refractory mutation system [ARMS]). Mutations were independently assessed by automated sequencing of genomic DNA amplified by polymerase chain reaction to evaluate the sensitivity and specificity of the ARMS assay. RESULTS: The ARMS assay correctly identified M6801, M694V, and V726A mutations in 82 persons with mutations documented by DNA sequencing (21 homozygotes, 2 compound heterozygotes, and 59 simple heterozygotes). Of 7 persons known from family studies to be noncarriers and 18 unrelated persons who were negative for these mutations by sequencing, none had MEFV mutations according to ARMS. CONCLUSION: The ARMS assay is a rapid, cost-effective, and accurate method for detecting three common mutations in familial Mediterranean fever.

Cross-Sectional Studies↗
PubMed1998

Widespread expression of serum amyloid A in histologically normal human tissues. Predominant localization to the epithelium.

Serum amyloid A (SAA) is an acute-phase reactant whose level in the blood is elevated to 1000-fold as part of the body's responses to various injuries, including trauma, infection, inflammation, and neoplasia. As an acute-phase reactant, the liver has been considered to be the primary site of expression. However, limited extrahepatic SAA expression was described in mouse tissues and in cells of human atherosclerotic lesions. Here we describe nonradioactive in situ hybridization experiments revealing that the SAA mRNA is widely expressed in many histologically normal human tissues. Expression was localized predominantly to the epithelial components of a variety of tissues, including breast, stomach, small and large intestine, prostate, lung, pancreas, kidney, tonsil, thyroid, pituitary, placenta, skin epidermis, and brain neurons. Expression was also observed in lymphocytes, plasma cells, and endothelial cells. RT-PCR analysis of selected tissues revealed expression of the SAA1, SAA2, and SAA4 genes but not of SAA3, consistent with expression of these genes in the liver. Immunohistochemical staining revealed SAA protein expression that co-localized with SAA mRNA expression. These data indicate local production of the SAA proteins in histologically normal human extrahepatic tissues.

Adult↗
PubMed1997

Functional analysis of a replication origin from Saccharomyces cerevisiae: identification of a new replication enhancer.

Yeast replication origins have a modular arrangement of essential DNA sequences containing the ARS consensus sequence (ACS) flanked by auxiliary DNA elements which stimulate origin function. One of the auxiliary elements identified at several origins is a DNA replication enhancer that binds the Abf1p protein. We have isolated an ARS sequence from Saccharomyces cerevisiae based on its ability to bind Abf1p. Here we present a detailed molecular dissection of this ARS, designated ARS 1501, and we demonstrate that it functions as a genomic replication origin on chromosome XV . Mutagenesis of the Abf1p DNA-binding sites revealed that these sequences did not contribute significantly to ARS function. Instead, a new DNA element important for replication, designated REN1501, has been located 5' to the T-rich strand of the ACS. We show that REN1501 functions in either orientation and at variable distances from the ACS, defining this element as a DNA replication enhancer. Most significantly, point mutations within this element decreased the stability of plasmids bearing ARS 1501, suggesting that REN1501 binds a protein important for replication initiation. Only three elements found at origins are known to specifically bind proteins. These include the ARS essential sequences and the Abf1p and Rap1p DNA-binding sites. We show that the function of REN1501 at the origin cannot be replaced by a Rap1p DNA-binding site or a site that binds the transcriptional factor Gal4p and can only be partially substituted for by an Abf1p recognition sequence. This implies that the role of the REN1501 element at the ARS 1501 origin is specific, and suggest that the frequency of origin firing in eukaryotic cells may be regulated by origin-specific enhancers.

Base Sequence↗
PubMed1997

An Abf1p C-terminal region lacking transcriptional activation potential stimulates a yeast origin of replication.

Although it has been demonstrated that eukaryotic cellular origins of DNA replication may harbor stimulatory elements that bind transcription factors, how these factors stimulate origin function is unknown. In Saccharomyces cerevisiae , the transcription factor Abf1p stimulates origin function of ARS121 and ARS1 . In the results presented here, an analysis of Abf1p function has been carried out utilizing LexA(BD)-Abf1p fusion proteins and an ARS 121 derivative harboring LexA DNA-binding sites. A minimal region which stimulates origin function mapped to 50 amino acids within the C-terminus of Abf1p. When tested for transcriptional activation of a LacZ reporter gene, the same LexA(BD)-Abf1p fusion protein had negligible transcriptional activation potential. Therefore, stimulation of ARS 121 may occur independently of a transcriptional activation domain. It has been previously observed that the Gal4p, Rap1p DNA-binding sites and the LexA-Gal4p fusion protein can replace the role of Abf1p in stimulating ARS 1 . Here we show that the stimulatory function of Abf1p at ARS 121 cannot be replaced by these alternative DNA-binding sites and the potent chimeric transcriptional activator LexA(BD)-Gal4(AD)p . Hence, these results strongly suggest that the Abf1p stimulation of replication may differ for ARS 121 and ARS 1 , and imply specificity in the Abf1p/ARS 121 relationship.

Bacterial Proteins↗
PubMed1997

Anatomic dissociation between HIV-1 and its endogenous inhibitor in mucosal tissues.

The rarity of oral transmission of human immunodeficiency virus (HIV)-1 by saliva suggests the absence of HIV-1 in the oral cavity and/or the presence of viral inhibitory molecules. We analyzed salivary gland tissues from 55 individuals with acquired immune deficiency syndrome (AIDS) for the presence of HIV-1 by in situ hybridization and detected the virus in more than 30% of these salivary glands. These data, together with previous demonstrations of HIV-1 in oral secretions, implicate a key role for an anti-viral molecule(s) in suppressing transmission. Thus, we focused on the characterization and localization of the endogenous antiviral molecule secretory leukocyte protease inhibitor (SLPI), which inhibits HIV-1 infection in vitro. Expression of SLPI transcripts was evident in submandibular, parotid, and minor salivary glands from both HIV-1-infected and seronegative subjects. Gene expression was reflected by similar levels of SLPI protein by immunohistochemical analysis in the tissues and by enzyme-linked immunosorbent assay in the saliva. However, although SLPI accumulated in acinar cells or ductal epithelium, HIV-1 transcripts did not, and these viral transcripts were identified only in mononuclear cells within the salivary gland stroma. By in situ hybridization, we found no evidence of productive HIV-1 infection of salivary gland epithelium. Thus, HIV-1 was frequently identified in salivary gland tissue, but the virus was found in interstitial mononuclear cells only and did not co-localize with SLPI. Once within the oral cavity, HIV-1 exposure to antiviral levels of SLPI may impede infection of additional target cells, contributing to the virtual absence of oral transmission of HIV-1 by saliva. These studies emphasize the importance of innate, endogenous inhibitors of HIV-1, particularly SLPI, as effective inhibitors of HIV-1 transmission.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Founder BRCA1 and BRCA2 mutations in Ashkenazi Jews in Israel: frequency and differential penetrance in ovarian cancer and in breast-ovarian cancer families.

Germ-line BRCA1 and BRCA2 mutations account for most of familial breast-ovarian cancer. In Ashkenazi Jews, there is a high population frequency (approximately 2%) of three founder mutations: BRCA1 185delAG, BRCA1 5382insC, and BRCA2 6174delT. This study examined the frequency of these mutations in a series of Ashkenazi women with ovarian cancer unselected for family history, compared with the frequency of these mutations in families ascertained on the basis of family history of at least two affected women. Penetrance was compared, both according to the method of family ascertainment (i.e., on the basis of an unselected ovarian cancer proband vs. on the basis of family history) and for the BRCA1 founder mutations compared with the BRCA2 6174delT mutation. There was a high frequency (10/22; [45%]) of germ-line mutations in Ashkenazi women with ovarian cancer, even in those with minimal or no family history (7/18 [39%]). In high-risk Ashkenazi families, a founder mutation was found in 59% (25/42). Families with any case of ovarian cancer were significantly more likely to segregate a founder mutation than were families with site-specific breast cancer. Penetrance was higher in families ascertained on the basis of family history than in families ascertained on the basis of an unselected proband, but this difference was not significant. Penetrance of BRCA1 185delAG and BRCA1 5382insC was significantly higher than penetrance of BRCA2 6174delT (hazard ratio 2.1 [95% CI 1.2-3.8]; two-tailed P = .01). Thus, the high rate of germ-line BRCA1/BRCA2 mutations in Ashkenazi women and families with ovarian cancer is coupled with penetrance that is lower than previously estimated. This has been shown specifically for the BRCA2 6174delT mutation, but, because of ascertainment bias, it also may be true for BRCA1 mutations.

Adult↗
PubMed1997

ApoA-I knockout mice: characterization of HDL metabolism in homozygotes and identification of a post-RNA mechanism of apoA-I up-regulation in heterozygotes.

The major high density lipoprotein (HDL) apolipoprotein, apoA-I, was knocked out by gene targeting in ES cells to provide a model for the study of HDL metabolism and its relationship to plasma and tissue cholesterol metabolism. HDL and non-HDL cholesterol (HDL-C) were reduced in apoA-I-deficient mice. Feeding a high fat-high cholesterol diet raised HDL-C minimally in apoA-I knockout compared to the large increase seen in control mice, suggesting an interaction between diet and apoA-I genotype. In apoA-I-deficient mice, HDL was normal in size but altered in composition. Compared to control mice there was more triglyceride and free cholesterol and less cholesteryl ester (CE), suggesting that apoA-I-deficient HDL is a poor substrate for hepatic lipase and lecithin:cholesterol acyltransferase (LCAT). The metabolic basis of the low HDL-C levels in the apoA-I knockout mice was decreased flux into the HDL CE pool. The absolute delivery of HDL CE to both peripheral tissues and liver was also decreased. As tissue cholesterol levels and synthesis were unchanged, the decreased flux of cholesterol into the HDL CE pool was most likely due to decreased efflux of cholesterol from the peripheral tissues and decreased functional LCAT activity. The low HDL-C state in the apoA-I-deficient mouse was associated with an absolute decrease in unidirectional transport of cholesterol from peripheral tissues to the liver but this did not lead to cholesterol accumulation in the periphery or a cholesterol deficit in the liver; nor was there altered peripheral tissue HMG-CoA reductase activity. The only sign of decreased cholesterol flux to the liver was a 2.3-fold decrease in liver cholesterol 7 alpha-hydroxylase mRNA, suggesting decreased bile acid synthesis. In the apoA-I knockout mouse model it appears that low HDL levels create a new steady state in which decreased cholesterol is delivered to both peripheral tissues and the liver.

Animals↗
PubMed1997

Intravenous drug compatibility: a challenge for the oncology nurse.

PURPOSE/OBJECTIVES: To examine the cause(s) and types of IV incompatibilities that can occur in the oncology population, to present information on commonly used oncologic medications, to identify resources available to nurses, and to provide specific interventions designed to prevent incompatibilities in various oncology settings. DATA SOURCES: Published articles, nursing and pharmacology textbooks. DATA SYNTHESIS: Many common oncologic medications are not compatible. A number of factors, including pH, drug additives, and cosolvents, may cause these incompatibilities. Incompatible reactions may be visually apparent or may occur on a molecular level. CONCLUSIONS: A basic understanding of incompatibilities can minimize their occurrence. A variety of resources and interventions are available. IMPLICATIONS FOR NURSING PRACTICE: Incompatibilities can occur easily in a variety of oncology settings and can result in detrimental medical and financial outcomes. Nurses play an important role in preventing incompatibilities. They must be familiar with the medications they are administering and have access to compatibility information and resources.

Antineoplastic Agents↗
PubMed1996

The Ku-like protein from Saccharomyces cerevisiae is required in vitro for the assembly of a stable multiprotein complex at a eukaryotic origin of replication.

We have previously shown that three distinct DNA-binding activities, in crude form, are necessary for the ATP-dependent assembly of a specific and stable multiprotein complex at a yeast origin of replication. Here we show the purification of one of these DNA binding activities, referred to as origin binding factor 2 (OBF2). The purified protein is a heterodimer composed of two polypeptides with molecular mass values of 65 and 80 kDa as determined by SDS/PAGE. Purified OBF2 not only binds DNA but also supports the formation of a protein complex at essential sequences within the ARS121 origin of replication. Interestingly, OBF2 binds tightly and nonspecifically to both duplex DNA and single-stranded DNA. The interaction with duplex DNA occurs at the termini. N-terminal sequencing of the 65-kDa subunit has revealed that this polypeptide is identical to the previously identified HDF1 peptide, a yeast homolog of the small subunit of the mammalian Ku autoantigen. Although the potential involvement of Ku in DNA metabolic events has been proposed, this is the first requirement for a Ku-like protein in the assembly of a protein complex at essential sequences within a eukaryotic origin of replication.

Animals↗
PubMed1996

Effect of patient characteristics on the yield of prolonged baseline head-up tilt testing and the additional yield of drug provocation.

OBJECTIVE: To define the value of tilt testing and hte additional yield of drug provocation over prolonged baseline tilt in different patient subgroups. (Many different protocols are in use for head-up tilt testing in heterogeneous groups of patients. Not all patients in reported series have recurrent syncope, and there is often a wide age range and a variable incidence of structural heart disease.) DESIGN: In a prospective study, baseline 60 degrees head-up tilt testing was undertaken for 45 minutes, initially without drug provocation. Patients who remained symptom free were given intravenous isoprenaline (isoproterenol) and further tilting or edrophonium (10 mg bolus) during tilt, in an order determined randomly before the start of the test. If they were symptom free after the first drug, they were given the other drug. A positive test was recorded when syncope or pre-syncope occurred with a rapid fall (> 30%) in blood pressure. The impact on tilt result of the type of symptoms, presence of significant structural heart disease (SHD), presence of a non-cardiovascular cause of sudden diminished consciousness (SDC), and age was then assessed by subgroup analysis. PATIENTS: 145 patients (73 female, mean age 51 (25), range 8-94) with one or more episodes of pre-syncope or syncope. RESULTS: 39 patients (27%, 21 female, age 49 (25) years) had positive tests and 106 (73%, 52 female, age 52 (25) years) negative tests. 27 (69%) had a positive test during baseline tilt at 20.5 (10.8) minutes, five (13%) with isoprenaline infusion, and seven (18%) with edrophonium bolus. Patients with recurrent syncope rather than single syncopal episodes or single or recurrent pre-syncope were more likely to have a positive tilt test (41% v 17%, P < 0.005) and patients with SHD or SDC (69/14 patients) were much less likely than patients without (16% v 42%, P < 0.0001). The yield of positive tests was similar if patients were below (26%) or above (27%) the mean age (50 years). When multiple factors were combined, the yield ranged from 0% for 21 patients under 50 years with SHD or SDC and without recurrent syncope to 73% in 11 patients over 50 years with recurrent syncope and no SHD or SDC. The additional yield in subgroups over 45 minute baseline tilt (70 (11)%) of isoprenaline (13 (10)%) was similar to that of edrophonium (17 (8)%, P = NS), but six (50% of those who were drug positive) patients required a second drug to produce a positive result (two with isoprenaline second, four with edrophonium second). CONCLUSIONS: Head-up tilt testing in a heterogeneous population has a low yield. Simple clinical characteristics define the type of patient who is likely to have a positive tilt test and the patient who is not and in whom other investigations should receive priority. The great majority of positive tests will occur during prolonged baseline testing if this is used. Isoprenaline and edrophonium produced similar additional yields of positive tests.

Age Factors↗
PubMed1996

The efficacy of pneumatic compression stockings in the prevention of pulmonary embolism after cardiac surgery.

INTRODUCTION: Pneumatic compression stocking (PCS) devices have been introduced to decrease the incidence of postoperative deep venous thrombosis (DVT). However, their role in the prophylaxis against pulmonary embolism (PE) remains unclear. This study was undertaken to compare the prophylactic effectiveness of subcutaneous heparin (SCH) alone vs the combined use of PCS and SCH in the prevention of PE following cardiac surgery. METHODS: We studied 2,551 consecutive patients who underwent cardiac surgery over a 10-year period. They were randomly allocated to two groups. Group A included 1,196 patients who were treated with 5,000 U of SCH every 12 h and group B included 1,355 patients treated with a combined prophylactic regimen of PCS and SCH. RESULTS: The diagnosis of PE was established in 69 patients by either high-probability ventilation perfusion scan, pulmonary angiogram, or autopsy. The incidence of PE in group A patients was 4% (48/1,196) and in group B was 1.5% (21/1,355). The concomitant use of bilateral PCS and SCH reduced the frequency of postoperative PE in 62% in comparison to the prophylaxis with SCH alone (p < 0.001). CONCLUSIONS: These data suggest that the combined prophylactic method of bilateral PCS and SCH is superior to SCH alone in the prevention of PE after cardiac surgery.

Aged↗
PubMed1996

Heparan sulfate-dependent and low density lipoprotein receptor-related protein-dependent catabolic pathways for lipoprotein lipase in mouse embryonic fibroblasts.

Heparan sulfate and low density lipoprotein receptor related protein (LRP) have been shown to participate in the uptake and degradation of the enzyme lipoprotein lipase (LPL). Yet, the contribution of each of these pathways to LPL metabolism and their possible dependence is unknown. In the present study we examined the metabolism of 125I-labeled LPL in untreated and heparinase-treated primary wild-type mouse embryonic fibroblasts (MEF) and in mouse fibroblasts that express single LRP allele (PEA-10) or are lacking the LRP (PEA-13). The degradation of LPL in PEA-13 cells was 30% lower than in MEF and PEA-10 cells. Heparinase treatment decreased the LPL degradation by 58%, 79% and 92%, whereas heparin reduced such degradation by 87%, 90% and 94% in MEF, PEA-10 and PEA-13 cultures, respectively. Assuming that a) heparinase treatment abolished the heparan-sulfate pathway, and that b) the degradation remaining in heparin-treated cultures represents nonspecific values, it appears that heparan sulfate contributes about 61%, 83% and 95% of total LPL degradation, whereas the LRP pathway contributes 39%, 17% and less than 5% of LPL degradation in MEF, PEA-10 and PEA-13 cells, respectively. In addition, the data indicate that LPL interaction with heparan sulfate and the LRP pathways is independent of each other. The study shows that these cells possess both a heparan sulfate-dependent pathway and an LRP-dependent pathway for LPL metabolism and that the two pathways are independent of each other.

Alleles↗
PubMed1995

ABF1 Ser-720 is a predominant phosphorylation site for casein kinase II of Saccharomyces cerevisiae.

ABF1 is a multifunctional phosphoprotein that binds specifically to yeast origins of replication and to transcriptional regulatory sites of a variety of genes. We isolated a protein kinase from extracts of Saccharomyces cerevisiae on the basis of its ability to specifically phosphorylate the ABF1 protein. Physical and biochemical properties of this kinase identify it as casein kinase II (CKII). The purified kinase has a high affinity for the ABF1 substrate as indicated by a relatively low Km value. Furthermore, when incubated with ABF1 and anti-ABF1 antibodies, the kinase forms an immunocomplex active in the phosphorylation of ABF1. Biochemical and genetic mapping localized a major site for phosphorylation at Ser-720 near the C terminus of the ABF1 protein. This serine is embedded within a domain enriched for acidic amino acid residues. A Ser-720 to Ala mutation abolishes phosphorylation by CKII in vitro. The same mutation also abolishes phosphorylation of this site in vivo, suggesting that CKII phosphorylates Ser-720 in vivo as well. Although three CKII enzymes, yeast, sea star, and recombinant human, utilize casein as a substrate with similar efficiencies, only the yeast enzyme efficiently phosphorylates the ABF1 protein. This suggests that ABF1 is a specific substrate of the yeast CKII and that this specificity may reside within one of the beta regulatory subunits of the enzyme. Thus, phosphorylation of ABF1 by yeast CKII may prove to be a useful system for studying targeting mechanisms of CKII to a physiological substrate.

Casein Kinase II↗