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R Lin

Publications and source records attributed to R Lin.

At least 91 records · Page 5Linked to original sources
PubMed1998

Transformation activity of Cdc42 requires a region unique to Rho-related proteins.

The Rho subfamily GTP-binding protein Cdc42 mediates actin cytoskeletal rearrangements and cell cycle progression and is essential for Ras transformation. Expression of a Cdc42 mutant (Cdc42(F28L)) that undergoes spontaneous activation (guanine nucleotide exchange) results in transformation of NIH3T3 fibroblasts. In this report, we show that deletion of residues 120-139 from Cdc42(F28L), which comprise an insert region unique to Rho subfamily proteins but is missing in other GTP-binding proteins, yields a Cdc42 molecule that still undergoes spontaneous GTP-GDP exchange and stimulates both actin cytoskeletal changes and the activation of the cellular targets p21-activated kinase and the c-Jun kinase (JNK1). However, this Cdc42 mutant is unable to transform cells. These findings indicate that the Rho subfamily insert region is dispensable for many of the known signaling pathways initiated by activated Cdc42 but is essential for its regulation of cell growth.

3T3 Cells↗
PubMed1998

Biochemical studies of the mechanism of action of the Cdc42-GTPase-activating protein.

The small GTP-binding proteins Rac, Rho, and Cdc42 were shown to mediate a variety of signaling pathways including cytoskeletal rearrangements, cell-cycle progression, and transformation. Key to the proper function of these GTP-binding proteins is an efficient shut-off mechanism that ensures the decay of the signal. Regulatory proteins termed GAPs (GTPase-activating proteins) enhance the intrinsic GTP hydrolysis of the GTP-binding proteins, thereby ensuring signal termination. We have used site-specific mutagenesis to elucidate the limit domain for GAP activity in Cdc42-GAP, and show that in addition to the known GAP-homology domain (three conserved boxes), a C-terminal region outside that domain is also essential for GAP activity. In addition, we have replaced the conserved arginine (Arg305), which was suggested by structural studies to be a key catalytic residue, with an alanine and found that the R305A Cdc42-GAP mutant has a greatly diminished catalytic capacity but is still able to bind Cdc42 with high affinity. Thus, a key catalytic role for this residue is confirmed. However, we also present evidence for the involvement of an additional residue(s), since the R305A Cdc42-GAP mutant still exhibits measurable activity. Some of this residual activity might result from a neighboring arginine, since a double mutant R305A/R306A shows a further decrease in catalytic activity.

Amino Acid Sequence↗
PubMed1998

A superrepressor mutant of the arginine repressor with a correctly predicted alteration of ligand binding specificity.

Arginine biosynthesis in Escherichia coli is negatively regulated by the hexameric repressor protein ArgR and the corepressor L-arginine. L-Arginine binds to ArgR in the C-terminal domain of the repressor. Binding to operator DNA occurs in the N-terminal domain. The molecular structures of both domains have recently been elucidated. The known stereochemistry of the arginine binding pocket was used for the rational design of a mutant ArgR with altered ligand specificity. Our prediction was that a replacement of Asp128 by asparagine would preferentially lead to the binding of L-citrulline, rather than L-arginine. The D128N mutant was constructed and was shown to fulfill our expectation by several experimental approaches. By isothermal titration calorimetry it was found to bind L-citrulline much more strongly than L-arginine, in contrast to wild-type ArgR. Exchange between the mutant trimers of the hexamer was inhibited by L-citrulline, as it is by L-arginine in the wild-type. The mutant protein was precipitated by L-citrulline but not by L-arginine, whereas the reverse is true for the wild-type protein. Demonstration of a corepressor action was, however, precluded by the superrepressor effect of the D128N mutation by itself. The mutant protein, in the absence of L-citrulline or L-arginine is as strong a repressor as the wild-type protein in the presence of L-arginine. We discuss two possible mechanisms, in terms of the known domain structures that could explain our observations.

Arginine↗
PubMed1998

Inducible expression of IkappaBalpha repressor mutants interferes with NF-kappaB activity and HIV-1 replication in Jurkat T cells.

Human immunodeficiency virus (HIV-1) utilizes the NF-kappaB/Rel proteins to regulate transcription through NF-kappaB binding sites in the HIV-1 long terminal repeat (LTR). Normally, NF-kappaB is retained in the cytoplasm by inhibitory IkappaB proteins; after stimulation by multiple activators including viruses, IkappaBalpha is phosphorylated and degraded, resulting in NF-kappaB release. In the present study, we examined the effect of tetracycline-inducible expression of transdominant repressors of IkappaBalpha (TD-IkappaBalpha) on HIV-1 multiplication using stably selected Jurkat T cells. TD-IkappaBalpha was inducibly expressed as early as 3 h after doxycycline addition and dramatically reduced both NF-kappaB DNA binding activity and LTR-directed gene activity. Interestingly, induced TD-IkappaBalpha expression also decreased endogenous IkappaBalpha expression to undetectable levels by 24 h after induction, demonstrating that TD-IkappaBalpha repressed endogenous NF-kappaB-dependent gene transcription. TD-IkappaBalpha expression also sensitized Jurkat cells to tumor necrosis factor-induced apoptosis. De novo HIV-1 infection of Jurkat cells was dramatically altered by TD-IkappaBalpha induction, resulting in inhibition of HIV-1 multiplication, as measured by p24 antigen, reverse transcriptase, and viral RNA. Given the multiple functions of the NF-kappaB/IkappaB pathway, TD-IkappaBalpha expression may interfere with HIV-1 multiplication at several levels: LTR-mediated transcription, Rev-mediated export of viral RNA, inhibition of HIV-1-induced pro-inflammatory cytokines, and increased sensitivity of HIV-1-infected cells to apoptosis.

Amino Acid Sequence↗
PubMed1998

Regulation of type I interferon gene expression by interferon regulatory factor-3.

The genes of the family of interferon (IFN) regulatory factors (IRF) encode DNA binding transcriptional factors that are involved in modulation of transcription of IFN and interferon-induced genes (ISG). The presence of IRF binding sites in the promoter region of IFNA and IFNB genes indicates that IRF factors recognizing these sites play an important role in the virus-mediated induction of these genes. We have described a novel human gene of this family, IRF-3, that is constitutively expressed in a variety of cell types. IRF-3 binds to the interferon-sensitive response element (ISRE) present in the ISG15 gene promoter and activates its transcriptional activity. In the present study, we examined whether IRF-3 can modulate transcriptional activity of IFNA and IFNB promoter regions. Our results demonstrate that IRF-3 can bind to the IRF-like binding sites present in the virus-inducible region of the IFNA4 promoter and to the PRDIII region of the IFNB promoter but cannot alone stimulate their transcriptional activity in the human cell line, 293. However, the fusion protein generated from the IRF-3 binding domain and the RelA(p65) activation domain effectively activates both IFNA4 and IFNB promoters. Cotransfection of IRF-3 and RelA(p65) expression plasmids activates the IFNB gene promoter but not the promoter of IFNA4 gene that does not contain the NF-kB binding site. Surprisingly, activation of the IFNA4 gene promoter by virus and IRF-1 in these cells was inhibited by IRF-3. These data indicate that in 293 cells IRF-3 does not stimulate expression of IFN genes but can cooperate with RelA(p65) to stimulate the IFNB promoter.

Amino Acid Sequence↗
PubMed1998

POP-1 and anterior-posterior fate decisions in C. elegans embryos.

Blastomeres in C. elegans embryos execute lineage programs wherein the fate of a cell is correlated reproducibly with the division sequence by which that cell is born. We provide evidence that the pop-1 gene functions to link anterior-posterior cell divisions with cell fate decisions. Each anterior cell resulting from an anterior-posterior division appears to have a higher level of nuclear POP-1 protein than does its posterior sister. Genes in the C. elegans Wnt pathway are required for this inequality in POP-1 levels. We show that loss of pop-1(+) activity leads to several types of anterior cells adopting the fates of their posterior sisters. These results suggest a mechanism for the invariance of blastomere lineages.

Animals↗
PubMed1998

Hepatocellular proliferation and development of hepatocellular carcinoma: a case-control study in chronic hepatitis C.

Patients with hepatitis C have an increased risk of developing hepatocellular carcinoma (HCC). This is related to the stage of chronic liver disease, as characterized histologically by hepatic fibrosis and architectural distortion, but it is unclear whether histological markers can define the risk of developing HCC. We conducted a case-control immunohistochemical study of Ki-67, a marker for hepatocellular proliferation, in livers of 18 patients who had developed HCC more than 2 years after the biopsy specimen had been taken. Using conditional logistic regression analysis, the results were compared with 18 selected controls, who were age-matched patients with hepatitis C of similar histological stage who had not developed HCC. We also examined livers for cellular dysplasia, p53 mutations, and bcl-2 overexpression, and assessed whether the results could be correlated with demographic and disease-related variables, such as gender, region of birth, alcohol consumption, severity of liver disease, HCV genotype, and markers of hepatitis B virus (HBV) infection. Livers from patients who developed HCC were more often positive for Ki-67 (13 of 18 [72%] v 9 of 18 [50%]; P = .06) and tended to have higher mean Ki-67 scores (6 +/- 7.5 v 3 +/- 4.4; P = .10) compared with control cases. In the HCC-predisposed group, three livers showed large cell dysplasia, two were positive for p53 mutations, and two for bcl-2 overexpression. In contrast, in the non-HCC group, only one case had dysplasia, and none were positive for immunostaining for p53 or bcl-2 mutations. With the exception of one case, all livers with large cell dysplasia or p53 mutations and bcl-2 overexpression were also positive for Ki-67. Twelve (55%) of the 22 Ki-67-positive cases were anti-HBc-positive in the serum, in contrast to 2 of 14 (14%) patients in the Ki-67-negative group (P = .01). Patients with evidence of past infection with HBV were more often Ki-67 positive than those who had no evidence of past infection (85% [11 of 13] v 45% [10 of 22]; P = .02). There were no other associations between demographic or disease-related variables and Ki-67 expression. Increased hepatocellular proliferative activity, as assessed by Ki-67 expression, may be one factor indicative of an increased risk of developing HCC among patients with chronic hepatitis C. Furthermore, past infection with HBV appears to be an important correlate of increased hepatocellular proliferation in hepatitis C.

Adult↗
PubMed1998

Effects of hepatitis G virus coinfection on severity of hepatitis C: relationship to risk factors and response to interferon treatment.

The aims of the present study were to identify characteristics that are more often associated with hepatitis G virus (HGV) coinfection in Australian patients infected with the hepatitis C virus (HCV) and to investigate the effects of HGV on the histological and functional severity of chronic hepatitis C. Serum samples from 209 patients with chronic hepatitis C were tested for HGV-RNA using single-round reverse transcriptase-polymerase chain reaction to primers directed at the NS5 region of the HGV genome. Hepatitis G virus RNA was detected in 40 cases (19%). Hepatitis G virus-coinfected patients tended to be younger and parenteral risks could be identified in all but six. Although country of birth did not differ significantly between the coinfected and HCV-alone groups, HGV-positive patients appeared to be less likely to have originated from Asia. On logistic regression analysis, HCV genotype 3a was found in a significantly higher proportion of patients with HGV coinfection than other genotypes (P < 0.01). Liver histology and response to interferon were similar in the HGV-coinfected and HCV-alone groups and liver-related complications appeared to occur less frequently in patients with both HGV and HCV. On univariate analysis, antipyrine clearance was found to be higher in the coinfected group (P < 0.05), implying better preservation of hepatic metabolic function, but this difference was lost when adjusted for HCV genotype. In conclusion, coinfection with HGV was more commonly associated with HCV genotype 3a, a genotype associated with injection drug use in younger patients. However, the presence of HGV coinfection did not adversely affect liver disease or the response to interferon treatment in patients with chronic hepatitis C.

Adult↗
PubMed1998

Molecular epidemiology of hepatitis C in Australia.

The aim of this study was to determine the distribution of hepatitis C virus (HCV) genotypes in Australian patients with hepatitis C and to identify factors associated with particular genotypes. Serum isolates of HCV-RNA were genotyped using a commercial oligonucleotide hybridization (line probe) assay. Relationships between demographic factors, mode of HCV transmission and HCV genotype were assessed by logistic regression analysis. Among 463 patients with hepatitis C, 425 tested positive for HCV-RNA and a single HCV genotype was identified in 420 cases. The patients' places of birth were Australia or New Zealand (62%), Asia (13%), Europe (12%), Mediterranean (6%), Middle East (6%) and other countries (< 1%). The most common genotypes were type 1 (52%) or type 3 (32%); type 2 (9.3%), type 4 (5.5%) and type 6 (1.7%) were less common. Patients with genotype 1b were older (48 +/- 13 years, P< 0.001) and patients with genotype 3 were younger than the remaining patients (37 +/- 11 years vs 42 +/- 12 years, P< 0.001). Among type 1 isolates, 1b was more common for patients born outside Australia compared with those born in Australia (50% vs 13%, P< 0.001) whereas non-1b subtypes were more common among Australian-born patients. Likewise, 21 of 23 (91%) patients with type 4 were from Egypt and six of seven (86%) with type 6 were from Vietnam. The relative importance of parenteral risk factors for HCV also varied according to geographic origin. Thus, a definite risk factor for HCV acquisition was identified in > 95% of Australian-born patients, but in only 33% of Asian or Mediterranean-born patients. Logistic regression analysis indicated that region of birth and risk factor (intravenous drug use or not) would allow 98% of type 4 cases and 76% of type 1b cases to be identified correctly. In summary, region of birth, patterns of migration over time and risk factors for transmission of HCV interact to determine the distribution of HCV genotypes in a multi-racial community like Australia.

Adult↗
PubMed1998

Group B Streptococcal septicaemia/meningitis in neonates in a Singapore teaching hospital.

Our aims were to establish the incidence and clinical characteristics of early and late onset Group B Streptococcal (GBS) septicaemia in neonates in our hospital over a period of 1 year. Routine screening for maternal GBS was not standard practice in the hospital. GBS was isolated from high vaginal swabs (HVS) obtained antenatally or postnatally for risk factors as determined by the obstetrician or neonatologist in charge. Data obtained were analyzed separately and these did not form part of the study. By a system of clinical case review and follow-up, mail, telephone and home visits, the outcome of all 15,062 livebirths in the hospital over a 1-year period were verified and reported. Our results show a low incidence of GBS infection in neonates in the hospital: early onset disease was 0.265 per 1,000 livebirths and late onset a quarter of that. The majority of our cases of early onset GBS disease were in premature infants. Because of our low incidence, prophylaxis schedules would have to ensure an acceptably smaller number of mothers exposed to antibiotics over and above the current level and the cooperation of our obstetricians. We have devised a schedule incorporating a current PROM (prelabour premature rupture of membranes) protocol which would result in only an additional 2.2% of mothers requiring prophylactic antibiotics.

Age of Onset↗
PubMed1998

Virus-dependent phosphorylation of the IRF-3 transcription factor regulates nuclear translocation, transactivation potential, and proteasome-mediated degradation.

The interferon regulatory factors (IRF) consist of a growing family of related transcription proteins first identified as regulators of the alpha beta interferon (IFN-alpha/beta) gene promoters, as well as the interferon-stimulated response element (ISRE) of some IFN-stimulated genes. IRF-3 was originally identified as a member of the IRF family based on homology with other IRF family members and on binding to the ISRE of the ISG15 promoter. IRF-3 is expressed constitutively in a variety of tissues, and the relative levels of IRF-3 mRNA do not change in virus-infected or IFN-treated cells. In the present study, we demonstrate that following Sendai virus infection, IRF-3 is posttranslationally modified by protein phosphorylation at multiple serine and threonine residues, which are located in the carboxy terminus of IRF-3. A combination of IRF-3 deletion and point mutations localized the inducible phosphorylation sites to the region -ISNSHPLSLTSDQ- between amino acids 395 and 407; point mutation of residues Ser-396 and Ser-398 eliminated virus-induced phosphorylation of IRF-3 protein, although residues Ser-402, Thr-404, and Ser-405 were also targets. Phosphorylation results in the cytoplasm-to-nucleus translocation of IRF-3, DNA binding, and increased transcriptional activation. Substitution of the Ser-Thr sites with the phosphomimetic Asp generated a constitutively active form of IRF-3 that functioned as a very strong activator of promoters containing PRDI-PRDIII or ISRE regulatory elements. Phosphorylation also appears to represent a signal for virus-mediated degradation, since the virus-induced turnover of IRF-3 was prevented by mutation of the IRF-3 Ser-Thr cluster or by proteasome inhibitors. Interestingly, virus infection resulted in the association of IRF-3 with the CREB binding protein (CBP) coactivator, as detected by coimmunoprecipitation with anti-CBP antibody, an interaction mediated by the C-terminal domains of both proteins. Mutation of residues Ser-396 and Ser-398 in IRF-3 abrogated its binding to CBP. These results are discussed in terms of a model in which virus-inducible, C-terminal phosphorylation of IRF-3 alters protein conformation to permit nuclear translocation, association with transcriptional partners, and primary activation of IFN- and IFN-responsive genes.

Amino Acid Sequence↗
PubMed1998

[Studies on QSAR of the antibacterial agents quinolones: changing the parent nucleus influenced the activity].

By the method of AM1, quantum chemistry indexes of 16 compounds of quinoline, 1,8-naphthyridine and pyrido(2,3-C)pyridazine analogues were calculated and 4 QSAR equations were obtained. The results showed that the net charge of 4-carbonyl oxygen is highly correlated with the antibacterial activity in vitro, the correlation coefficient of the regressions are high(R > or = 0.96). The antibacterial activity in vitro is strongly influenced by the coplanarity of 3-carboxylic acid and the parent nucleus. In light of this study, a new parent nucleus of isothiazoleannexed quinolizine was proposed, which is expected to have much higher activity.

Bacteria↗
PubMed1997

A novel Cdc42Hs mutant induces cellular transformation.

Cdc42Hs is a small GTPase of the Rho-subfamily, which regulates signaling pathways that influence cell morphology and polarity, cell-cycle progression and transcription. An essential role for Cdc42Hs in cell growth regulation has been suggested by the finding that the Dbl oncoprotein is an upstream activator-a guanine nucleotide exchange factor (GEF)-for Cdc42Hs, and that activated mutants of the closely related GTPases Rac and Rho are transforming. As we were unable to obtain significant over-expression of GTPase-defective Cdc42Hs mutants, we have generated a mutant, Cdc42Hs(F28L), which can undergo spontaneous GTP-GDP exchange while maintaining full GTPase activity, and thus should exhibit functional activities normally imparted by Dbl. In cultured fibroblasts, Cdc42Hs(F28L) activated the c-Jun kinase (JNK1) and stimulated filopodia formation. Cells stably expressing Cdc42Hs(F28L) also exhibited several hallmarks of transformation-reduced contact inhibition, lower dependence on serum for growth, and anchorage-independent growth. Our findings indicate that Cdc42Hs plays a role in cell proliferation, and is a likely physiological mediator of Dbl-induced transformation.

3T3 Cells↗
PubMed1997

Activation of multiple growth regulatory genes following inducible expression of IRF-1 or IRF/RelA fusion proteins.

Interferon Regulatory Factor (IRF)-1 has been characterized as an important growth regulatory and immunomodulatory transcription factor. To further characterize the potential targets of IRF-1 antiproliferative activity, IRF-1 was expressed under the control of the tetracycline-inducible system in murine NIH3T3 cells. Due to their ability to mimic IRF-1 transactivator function, the regulatory potential of IRF-1/RelA and IRF-2/RelA fusion proteins consisting of the DNA binding domains of IRF-1 or IRF-2 fused to the transactivation domain of NF-kappaB RelA(p65) was also examined. Cells inducibly expressing IRF-1 or IRF/RelA in response to doxycycline treatment displayed significantly reduced growth rates compared to control cells, and inhibition of cell growth correlated directly with the level of transgene expression. Interestingly, IRF-1 and IRF/RelA expression also induced a low level of apoptosis, as detected by microscopic analyses. Furthermore, expression of the interferon inducible, double stranded RNA dependent kinase PKR was increased following IRF-1 or IRF/RelA induction. Most strikingly, induction of IRF-1 and IRF/RelA expression resulted in a significant increase in STAT1 (p91) protein and increased ISGF3 DNA binding activity, suggesting that IRF-1 tumor suppressor activity may involve a novel mechanism which activates the JAK-STAT pathway through STAT1. WAF1 levels were also constitutively elevated in IRF-1 and IRF-1/RelA cells. These studies demonstrate that inducible expression of the transactivation function of IRF-1 or IRF/RelA mediates tumor suppressor activity by inducing cell growth arrest, apoptosis and the differential activation of growth regulatory genes such as PKR, STAT1 and WAF1.

3T3 Cells↗
PubMed1997

Wnt signaling and an APC-related gene specify endoderm in early C. elegans embryos.

In a 4-cell stage C. elegans embryo, signaling by the P2 blastomere induces anterior-posterior polarity in the adjacent EMS blastomere, leading to endoderm formation. We have taken genetic and reverse genetic approaches toward understanding the molecular basis for this induction. These studies have identified a set of genes with sequence similarity to genes that have been shown to be, or are implicated in, Wnt/Wingless signaling pathways in other systems. The C. elegans genes described here are related to wnt/wingless, porcupine, frizzled, beta-catenin/armadillo, and the human adenomatous polyposis coli gene, APC. We present evidence that there may be partially redundant inputs into endoderm specification and that a subset of these genes appear also to function in determining cytoskeletal polarity in certain early blastomeres.

Adenomatous Polyposis Coli Protein↗
PubMed1997

Selective interaction of hsp90 with an estrogen receptor ligand-binding domain containing a point mutation.

The 90-kDa heat shock protein (hsp90) has been implicated in modulating steroid receptor function in vitro and in vivo. Previous studies have suggested that hsp90 interacts with large portions of the estrogen receptor (ER) ligand-binding domain and sequences of the receptor required for stable DNA binding. To characterize the interaction of the ER ligand-binding domain with hsp90, we have compared the properties of chimeras created by coupling the ligand-binding domain to the constitutive transactivator VP16-GAL. Two types of chimeras were created: VP16-GAL-ERG, containing the wild-type ligand-binding domain derived from the cDNA HEG0, and VP16-GAL-ERV, containing the substitution G400V derived from the ligand-binding domain of the original ER cDNA isolate, HE0. The G400V mutation alters the physical properties of VP16-GAL-ERV by rendering it hormone-dependent for DNA binding and more strongly dependent on estradiol for transactivation compared with VP16-GAL-ERG. Glycerol gradient analyses and chemical cross-linking/coimmunoprecipitation showed that, unlike VP16-GAL-ERG, VP16-GAL-ERV formed stable complexes with hsp90 in vitro. These data show that hsp90 selectively recognizes the altered ER ligand-binding domain containing the G400V substitution and indicate that the wild-type ER ligand-binding domain of VP16-GAL-ERG does not interact with hsp90 in vitro. Hormone binding studies showed that the ligand-binding domain of VP16-GAL-ERV was destabilized by incubation in the presence of high concentrations of salt or in the absence of sodium molybdate, conditions that disrupt its interaction with hsp90. The ligand-binding domain of the Val-400 ER thus behaves similarly to that of the wild-type glucocorticoid receptor, which has previously been shown to interact with hsp90 in vitro. These results provide evidence for the action of hsp90 as a molecular chaperone by selectively recognizing destabilized proteins.

Animals↗
PubMed1997

The exchange between proglycogen and macroglycogen and the metabolic role of the protein-rich glycogen in rat skeletal muscle.

The aim of this study is to determine if proglycogen and macroglycogen are kinetically related in rat skeletal muscle. Eight groups of anesthetized fasted rats (seven hepatic-occluded and one nonoccluded) were intravenously infused with [3-3H]glucose at a rate of 1.7 microCi x min(-1) for 20 min. At the end of infusion, hindlimb muscles were excised and rapidly frozen in liquid nitrogen. Proglycogen was extracted by precipitation in 10% TCA; and macroglycogen as a part of total glycogen by precipitation in 20% KOH-65% ethanol. Along with the tracer, the occluded rats were also infused with: saline (group 1); insulin at rates ranging from 5 to 50 mU x min(-1) (groups 2 to 5); and insulin at a rate of 10 mU x min(-1) plus glucose at rates of 10.2 and 20.4 micromol x min(-1), respectively (groups 6 and 7). The infusion regimens resulted in up to 30-fold difference in whole-body glucose utilization among the rats. In the rats infused with saline and insulin at a rate of 5 mU x min(-1), [3H]glucose was found to be exclusively incorporated into proglycogen. Incorporation into macroglycogen was found in the rats infused with insulin at rates > 10 mU x min(-1). Supplementary glucose infusion increased the synthesis of [3H]proglycogen (four- to sixfold), and equilibrated the two extractable forms of glycogen in the insulin-infused rats. In the saline-infused nonoccluded rats, only proglycogen was found to be labeled. In conclusion, our data indicate that in the intact and hepatic-occluded rats, proglycogen in the skeletal muscles may undergo synthesis and degradation of its own more readily than exchange between itself and depot macroglycogen.

Animals↗