Log in

Relevant bibliographies by topics / Igf1r knockout / Journal articles

To see the other types of publications on this topic, follow the link: Igf1r knockout.

Journal articles on the topic 'Igf1r knockout'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Igf1r knockout.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Müller, Kathrin, Dagmar Führer, Jens Mittag, et al. "TSH Compensates Thyroid-Specific IGF-I Receptor Knockout and Causes Papillary Thyroid Hyperplasia." Molecular Endocrinology 25, no. 11 (2011): 1867–79. http://dx.doi.org/10.1210/me.2011-0065.

Full text

Abstract:

Abstract Although TSH stimulates all aspects of thyroid physiology IGF-I signaling through a tyrosine kinase-containing transmembrane receptor exhibits a permissive impact on TSH action. To better understand the importance of the IGF-I receptor in the thyroid in vivo, we inactivated the Igf1r with a Tg promoter-driven Cre-lox system in mice. We studied male and female mice with thyroidal wild-type, Igf1r+/−, and Igf1r−/− genotypes. Targeted Igf1r inactivation did transiently reduce thyroid hormone levels and significantly increased TSH levels in both heterozygous and homozygous mice without af

APA, Harvard, Vancouver, ISO, and other styles

2

Cookman, Clifford J., та Scott M. Belcher. "Estrogen Receptor-β Up-Regulates IGF1R Expression and Activity to Inhibit Apoptosis and Increase Growth of Medulloblastoma". Endocrinology 156, № 7 (2015): 2395–408. http://dx.doi.org/10.1210/en.2015-1141.

Full text

Abstract:

Medulloblastoma (Med) is the most common malignant brain tumor in children. The role of ESR2 [estrogen receptor (ER)-β] in promoting Med growth was comprehensively examined in three in vivo models and human cell lines. In a novel Med ERβ-null knockout model developed by crossing Esr2−/− mice with cerebellar granule cell precursor specific Ptch1 conditional knockout mice, the tumor growth rate was significantly decreased in males and females. The absence of Esr2 resulted in increased apoptosis, decreased B-cell lymphoma 2 (BCL2), and IGF-1 receptor (IGF1R) expression, and decreased levels of ac

APA, Harvard, Vancouver, ISO, and other styles

3

McMullen, Julie R., Tetsuo Shioi, Li Zhang, et al. "Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy." Molecular and Cellular Biology 24, no. 14 (2004): 6231–40. http://dx.doi.org/10.1128/mcb.24.14.6231-6240.2004.

Full text

Abstract:

ABSTRACT Ribosomal S6 kinases (S6Ks) have been depicted as critical effectors downstream of growth factor pathways, which play an important role in the regulation of protein synthesis by phosphorylating the ribosomal protein, S6. The goal of this study was to determine whether S6Ks regulate heart size, are critical for the induction of cardiac hypertrophy in response to a pathological or physiological stimulus, and whether S6Ks are critical downstream effectors of the insulin-like growth factor 1 (IGF1)-phosphoinositide 3-kinase (PI3K) pathway. For this purpose, we generated and characterized

APA, Harvard, Vancouver, ISO, and other styles

4

Wang, Linlin, Thomas C. Schulz, Eric S. Sherrer, et al. "Self-renewal of human embryonic stem cells requires insulin-like growth factor-1 receptor and ERBB2 receptor signaling." Blood 110, no. 12 (2007): 4111–19. http://dx.doi.org/10.1182/blood-2007-03-082586.

Full text

Abstract:

Abstract Despite progress in developing defined conditions for human embryonic stem cell (hESC) cultures, little is known about the cell-surface receptors that are activated under conditions supportive of hESC self-renewal. A simultaneous interrogation of 42 receptor tyrosine kinases (RTKs) in hESCs following stimulation with mouse embryonic fibroblast (MEF) conditioned medium (CM) revealed rapid and prominent tyrosine phosphorylation of insulin receptor (IR) and insulin-like growth factor-1 receptor (IGF1R); less prominent tyrosine phosphorylation of epidermal growth factor receptor (EGFR) fa

APA, Harvard, Vancouver, ISO, and other styles

5

Wong, Wei. "Protein homeostasis limiting cancer." Science Signaling 9, no. 411 (2016): ec12-ec12. http://dx.doi.org/10.1126/scisignal.aaf2516.

Full text

Abstract:

There is interest in targeting protein quality control pathways that ensure refolding or elimination of misfolded proteins to kill cancer cells. Osorio et al. identified a role for AIRAPL (an ortholog of AIP-1, which is involved in protein quality control pathways in Caenorhabditis elegans) in myeloproliferative neoplasms, a group of diseases in which the production of blood cells in the bone marrow is increased. Mice lacking Zfand2b (the gene encoding AIRAPL) developed hematological symptoms characteristic of myeloproliferative neoplasms, such as splenomegaly and expansion of various myeloid

APA, Harvard, Vancouver, ISO, and other styles

6

Young, Kira, Elizabeth Eudy, Matthew Loberg, Rebecca Bell, and Jennifer Trowbridge. "Decline in Insulin-like Growth Factor-1 (IGF1) from Aged Mesenchymal Stromal Cells Is a Targetable Mechanism to Rescue Hematopoietic Stem Cell Aging." Blood 134, Supplement_1 (2019): 526. http://dx.doi.org/10.1182/blood-2019-124534.

Full text

Abstract:

Hematopoietic stem cells (HSCs) are responsible for long-term maintenance and regeneration of the hematopoietic system. Loss of long-term (LT)-HSC function is a major contributor to decline in hematopoietic function with aging, leading to increased risk of infection, poor vaccination response, and increased susceptibility to hematologic malignancies. A number of LT-HSC-intrinsic alterations and LT-HSC-extrinsic changes in the bone marrow (BM) microenvironment have been associated with functional decline in aged LT-HSCs. Outstanding questions in the field are which of these mechanisms cause, ra

APA, Harvard, Vancouver, ISO, and other styles

7

Xie, Ying, Xin Hu, and Zhe Li. "Developmental Stage and Sex-Specific Role of IGF/IGF1R Signaling in Hematopoietic Stem and Progenitor Cells." Blood 126, no. 23 (2015): 1157. http://dx.doi.org/10.1182/blood.v126.23.1157.1157.

Full text

Abstract:

Abstract Insulin-like growth factors (IGFs) are critical regulators of cell growth, proliferation and survival. Their activities are mainly mediated through insulin-like growth factor 1 receptor (IGF1R). Both IGFs and IGF1R are commonly involved in human cancers, including leukemia. Thus, a better understanding of the role of IGF/IGF1R signaling in normal hematopoiesis will enhance our understanding of leukemogenesis. We showed previously a developmental stage-specific role of this pathway in regulating fetal (but not adult) megakaryocytic progenitors via interplay with GATA1 (Genes Dev. 24:16

APA, Harvard, Vancouver, ISO, and other styles

8

Natalishvili, Natalia, Magnus Axelson, Leonard Girnita, Olle Larsson та Daiana Vasilcanu. "Aberrant intracellular IGF-1R β-subunit makes receptor knockout cells (IGF1R-/-) susceptible to oncogenic transformation". Experimental Cell Research 315, № 8 (2009): 1458–67. http://dx.doi.org/10.1016/j.yexcr.2009.01.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Osuka, Satoru, Dan Zhu, Zhaobin Zhang, et al. "STEM-16. IGF1/N-CADHERIN/b-CATENIN/CLUSTERIN SIGNALING AXIS MEDIATES ADAPTIVE RADIORESISTANCE IN GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (2020): ii199. http://dx.doi.org/10.1093/neuonc/noaa215.833.

Full text

Abstract:

Abstract Glioblastoma (GBM) is composed of heterogeneous tumor cell populations including those with stem cell properties, termed glioma stem cells (GSCs). GSCs are innately less radiation sensitive than the tumor bulk and are believed to drive GBM formation and recurrence after repeated irradiation. However, it is unclear how GSCs adapt to escape the toxicity of repeated irradiation used in clinical practice. To identify important mediators of adaptive radioresistance, we generated radioresistant human and mouse GSCs by exposing them to repeat cycles of irradiation. Surviving subpopulations a

APA, Harvard, Vancouver, ISO, and other styles

10

Wu, Shufang, Wei Yang, and Francesco De Luca. "Insulin-Like Growth Factor-Independent Effects of Growth Hormone on Growth Plate Chondrogenesis and Longitudinal Bone Growth." Endocrinology 156, no. 7 (2015): 2541–51. http://dx.doi.org/10.1210/en.2014-1983.

Full text

Abstract:

GH stimulates growth plate chondrogenesis and longitudinal bone growth directly at the growth plate. However, it is not clear yet whether these effects are entirely mediated by the local expression and action of IGF-1 and IGF-2. To determine whether GH has any IGF-independent growth-promoting effects, we generated TamCartIgf1rflox/flox mice. The systemic injection of tamoxifen in these mice postnatally resulted in the excision of the IGF-1 receptor (Igf1r) gene exclusively in the growth plate. TamCartIgf1rflox/flox tamoxifen-treated mice [knockout (KO) mice] and their Igf1rflox/flox control li

APA, Harvard, Vancouver, ISO, and other styles

11

Li, Lijun, Marcus Byrd, Kwame Doh, et al. "Absence of renal enlargement in fructose-fed proximal-tubule-select insulin receptor (IR), insulin-like-growth factor receptor (IGF1R) double knockout mice." Physiological Reports 4, no. 23 (2016): e13052. http://dx.doi.org/10.14814/phy2.13052.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Lovat, Francesca, Matteo Fassan, Pierluigi Gasparini, et al. "miR-15b/16-2 deletion promotes B-cell malignancies." Proceedings of the National Academy of Sciences 112, no. 37 (2015): 11636–41. http://dx.doi.org/10.1073/pnas.1514954112.

Full text

Abstract:

The central role of the microRNA (miR) 15a/16-1 cluster in B-cell oncogenesis has been extensively demonstrated, with over two-thirds of B-cell chronic lymphocytic leukemia characterized by the deletion of the miR-15a/16-1 locus at 13q14. Despite the well-established understanding of the molecular mechanisms occurring during miR-15a/16-1 dysregulation, the oncogenic role of other miR-15/16 family members, such as the miR-15b/16-2 cluster (3q25), is still far from being elucidated. Whereas miR-15a is highly similar to miR-15b, miR-16-1 is identical to miR-16-2; thus, it could be speculated that

APA, Harvard, Vancouver, ISO, and other styles

13

Heitzeneder, Sabine, Elena Sotillo, Jack F. Shern, et al. "Pregnancy-Associated Plasma Protein-A (PAPP-A) in Ewing Sarcoma: Role in Tumor Growth and Immune Evasion." JNCI: Journal of the National Cancer Institute 111, no. 9 (2019): 970–82. http://dx.doi.org/10.1093/jnci/djy209.

Full text

Abstract:

AbstractBackgroundEwing sarcoma (EWS) manifests one of the lowest somatic mutation rates of any cancer, leading to a scarcity of druggable mutations and neoantigens. Immunotherapeutics targeting differentially expressed cell surface antigens could provide therapeutic benefit for such tumors. Pregnancy-associated plasma protein A (PAPP-A) is a cell membrane-associated proteinase produced by the placenta that promotes fetal growth by inducing insulinlike growth factor (IGF) signaling.MethodsBy comparing RNA expression of cell surface proteins in EWS (n = 120) versus normal tissues (n = 42), we c

APA, Harvard, Vancouver, ISO, and other styles

14

Tang, Huihui, Ricardo De Matos Simoes, Ryosuke Shirasaki, et al. "CRISPR Activation Screen for Drivers of MM Cell Proliferation." Blood 132, Supplement 1 (2018): 3197. http://dx.doi.org/10.1182/blood-2018-99-118712.

Full text

Abstract:

Abstract CRISPR/Cas9-based gene editing has become a powerful tool for loss-of-function (LOF) studies and has allowed us to systematically interrogate the function of genes regulating the survival and proliferation of multiple myeloma (MM) cells in vitro, in vivo and in the context of treatment resistance (e.g. De Matos Simoes et al., Shirasaki et al., and Gandolfi et al. ASH 2017). We reasoned, however, that important additional information can be obtained from CRISPR-based gain-of-function (GOF) approaches which can achieve transcriptional activation at endogenous genomic loci. We thus perfo

APA, Harvard, Vancouver, ISO, and other styles

15

Zheng, Yu, Yongli Song, Qi Han, et al. "Intestinal epithelial cell-specific IGF1 promotes the expansion of intestinal stem cells during epithelial regeneration and functions on the intestinal immune homeostasis." American Journal of Physiology-Endocrinology and Metabolism 315, no. 4 (2018): E638—E649. http://dx.doi.org/10.1152/ajpendo.00022.2018.

Full text

Abstract:

It is well known that insulin-like growth factor 1 (IGF1) acts as a trophic factor in small intestine under both physiological and pathophysiological conditions. However, it still lacks direct in vivo evidence of the functions of intestinal epithelial cell (IEC)-specific IGF1 under both normal and pathological conditions. Using IEC-specific IGF1-knockout (cKO) mice and Lgr5-eGFP-CreERT mice, we demonstrate that IEC-specific IGF1 can enhance nutrient uptake, reduce protein catabolism and energy consumption, and promote the proliferation and expansion of intestinal epithelial cells, including in

APA, Harvard, Vancouver, ISO, and other styles

16

William Lau, K. H., David J. Baylink, Xiao-Dong Zhou, et al. "Osteocyte-derived insulin-like growth factor I is essential for determining bone mechanosensitivity." American Journal of Physiology-Endocrinology and Metabolism 305, no. 2 (2013): E271—E281. http://dx.doi.org/10.1152/ajpendo.00092.2013.

Full text

Abstract:

This study sought to determine whether deficient Igf1 expression in osteocytes would affect loading-induced osteogenic response. Tibias of osteocyte Igf1 conditional knockout (KO) mice (generated by cross-breeding Igf1 floxed mice with Dmp1- Cre transgenic mice) and wild-type (WT) littermates were subjected to four-point bending for 2 wk. Microcomputed tomography confirmed that the size of tibias of conditional mutants was smaller. Loading with an equivalent loading strain increased periosteal woven bone and endosteal lamellar bone formation in WT mice but not in conditional KO mice. Consisten

APA, Harvard, Vancouver, ISO, and other styles

17

Viana-Huete, Vanesa, Carlos Guillén, Ana García-Aguilar, et al. "Essential Role of IGFIR in the Onset of Male Brown Fat Thermogenic Function: Regulation of Glucose Homeostasis by Differential Organ-Specific Insulin Sensitivity." Endocrinology 157, no. 4 (2016): 1495–511. http://dx.doi.org/10.1210/en.2015-1623.

Full text

Abstract:

Abstract Brown fat is a thermogenic tissue that generates heat to maintain body temperature in cold environments and dissipate excess energy in response to overfeeding. We have addressed the role of the IGFIR in the brown fat development and function. Mice lacking IGFIR exhibited normal brown adipose tissue/body weight in knockout (KO) vs control mice. However, lack of IGFIR decreased uncoupling protein 1 expression in interscapular brown fat and beige cells in inguinal fat. More importantly, the lack of IGFIR resulted in an impaired cold acclimation. No differences in the total fat volume wer

APA, Harvard, Vancouver, ISO, and other styles

18

Frantsiyants, E. M., I. V. Kaplieva, I. V. Neskubina, et al. "Influence of urokinase gene-knockout in C57BL/6-PlautmI. IBugThisPlau6FDhu/GFDhu mice on growth factors in malignant melanoma." Research and Practical Medicine Journal 7, no. 1 (2020): 25–37. http://dx.doi.org/10.17709/2409-2231-2020-7-1-3.

Full text

Abstract:

Purpose of the study. Studying characteristics of the growth factor dynamics in the intact skin, tumors and perifocal tissues of melanoma in urokinase (uPA) gene-knockout mice.Materials and methods. The study included male and female С57 ВL/6 mice (n=47) and C57BL/6‑Plautm1.1BugThisPlauGFDhu/GFDhu mice with uPA gene-knockout (n=31). В16/F10 melanoma was transplanted subcutaneously at a dose of 0.5 mL (1:10 in normal saline). Intact mice of the same strain served as controls. Levels of VEGFA, VEGFC, sVEGFR1, sVEGFR3, IGF1, IGF2, TGFβ1 and FGF21 were determined by ELISA in the skin, tumor and pe

APA, Harvard, Vancouver, ISO, and other styles

19

Hikake, Tamiki, Shinji Hayashi, Taisen Iguchi, and Tomomi Sato. "The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary." Journal of Endocrinology 203, no. 2 (2009): 231–40. http://dx.doi.org/10.1677/joe-09-0232.

Full text

Abstract:

IGF1 knockout (IGF1KO) mice show a reduced number of prolactin (PRL) producing cells (PRL cells); however, the role of IGF1 in PRL cell proliferation and differentiation in immature mice is unclear. In this study, ontogenic changes in the percentages of PRL cells, GH producing cells (GH cells), and 5-bromo-2′-deoxyuridine (BrdU)-labeled cells in the anterior pituitary of male IGF1KO mice during the postnatal period were investigated. The percentage of PRL cells in IGF1KO mice was significantly lower at day 20 compared with that in wild-type (WT) mice, while GH cells in IGF1KO mice were signifi

APA, Harvard, Vancouver, ISO, and other styles

20

Gahete, Manuel D., José Córdoba-Chacón, Qing Lin, et al. "Insulin and IGF-I Inhibit GH Synthesis and Release in Vitro and in Vivo by Separate Mechanisms." Endocrinology 154, no. 7 (2013): 2410–20. http://dx.doi.org/10.1210/en.2013-1261.

Full text

Abstract:

Abstract IGF-I is considered a primary inhibitor of GH secretion. Insulin may also play an important role in regulating GH levels because insulin, like IGF-I, can suppress GH synthesis and release in primary pituitary cell cultures and insulin is negatively correlated with GH levels in vivo. However, understanding the relative contribution insulin and IGF-I exert on controlling GH secretion has been hampered by the fact that circulating insulin and IGF-I are regulated in parallel and insulin (INSR) and IGF-I (IGFIR) receptors are structurally/functionally related and ubiquitously expressed. To

APA, Harvard, Vancouver, ISO, and other styles

21

Viana-Huete, Vanesa, Carlos Guillén, Gema García, et al. "Male Brown Fat–Specific Double Knockout of IGFIR/IR: Atrophy, Mitochondrial Fission Failure, Impaired Thermogenesis, and Obesity." Endocrinology 159, no. 1 (2017): 323–40. http://dx.doi.org/10.1210/en.2017-00738.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Tang, Huihui, Ryosuke Shirasaki, Ricardo De Matos Simoes, et al. "Functional Characterization of Genes Driving Enhanced Biological Aggressiveness of Myeloma Cells: Identification of Novel and Understudied "Drivers" of Myeloma." Blood 134, Supplement_1 (2019): 313. http://dx.doi.org/10.1182/blood-2019-128919.

Full text

Abstract:

Loss-of-function (LOF) studies (e.g. using RNAi or CRISPR) have historically been the main functional approaches to identify and study genes which drive the biology of Multiple Myeloma(MM) or other neoplasias. We hypothesized though that substantial complementary data can be derived from systematically examining the impact of transcriptional activation of endogenous genomic loci of different genes. To perform such gain-of-function (GOF) studies in an open-ended genome-scale manner, we applied CRISPR activation approaches in 4 MM lines (MM1S, KMS11, LP1, L363) which were transduced with the dCa

APA, Harvard, Vancouver, ISO, and other styles

23

Dobie, R., V. E. MacRae, C. Huesa, R. van't Hof, S. F. Ahmed, and C. Farquharson. "Direct stimulation of bone mass by increased GH signalling in the osteoblasts of Socs2−/− mice." Journal of Endocrinology 223, no. 1 (2014): 93–106. http://dx.doi.org/10.1530/joe-14-0292.

Full text

Abstract:

The suppressor of cytokine signalling (Socs2−/−)-knockout mouse is characterised by an overgrowth phenotype due to enhanced GH signalling. The objective of this study was to define theSocs2−/−bone phenotype and determine whether GH promotes bone mass via IGF1-dependent mechanisms. Despite no elevation in systemic IGF1 levels, increased body weight in 4-week-oldSocs2−/−mice following GH treatment was associated with increased cortical bone area (Ct.Ar) (P<0.01). Furthermore, detailed bone analysis of male and female juvenile and adultSocs2−/−mice revealed an altered cortical and trabecular p

APA, Harvard, Vancouver, ISO, and other styles

24

Shefi-Friedman, Liat, Efrat Wertheimer, Shlomzion Shen, Asia Bak, Domenico Accili, and Sanford R. Sampson. "Increased IGFR activity and glucose transport in cultured skeletal muscle from insulin receptor null mice." American Journal of Physiology-Endocrinology and Metabolism 281, no. 1 (2001): E16—E24. http://dx.doi.org/10.1152/ajpendo.2001.281.1.e16.

Full text

Abstract:

We have studied the role of the insulin receptor (IR) in metabolic and growth-promoting effects of insulin on primary cultures of skeletal muscle derived from the limb muscle of IR null mice. Cultures of IR null skeletal muscle displayed normal morphology and spontaneous contractile activity. Expression of muscle-differentiating proteins was slightly reduced in myoblasts and myotubes of the IR null skeletal muscle cells, whereas that of the Na+/K+ pump appeared to be unchanged. Insulin-like growth factor receptor (IGFR) expression was higher in myoblasts from IR knockout (IRKO) than from IR wi

APA, Harvard, Vancouver, ISO, and other styles

25

DeMambro, Victoria E., Masanobu Kawai, Thomas L. Clemens, et al. "A novel spontaneous mutation of Irs1 in mice results in hyperinsulinemia, reduced growth, low bone mass and impaired adipogenesis." Journal of Endocrinology 204, no. 3 (2009): 241–53. http://dx.doi.org/10.1677/joe-09-0328.

Full text

Abstract:

A spontaneous mouse mutant, designated ‘small’ (sml), was recognized by reduced body size suggesting a defect in the IGF1/GH axis. The mutation was mapped to the chromosome 1 region containing Irs1, a viable candidate gene whose sequence revealed a single nucleotide deletion resulting in a premature stop codon. Despite normal mRNA levels in mutant and control littermate livers, western blot analysis revealed no detectable protein in mutant liver lysates. When compared with the control littermates, Irs1sml/Irs1sml (Irs1sml/sml) mice were small, lean, hearing impaired; had 20% less serum IGF1; w

APA, Harvard, Vancouver, ISO, and other styles

26

Ahmed, S. F., and C. Farquharson. "The effect of GH and IGF1 on linear growth and skeletal development and their modulation by SOCS proteins." Journal of Endocrinology 206, no. 3 (2010): 249–59. http://dx.doi.org/10.1677/joe-10-0045.

Full text

Abstract:

Circulating signalling proteins have often been divided into hormones and cytokines, but it is increasingly being recognised that these substances have a number of common characteristics and mechanisms of action. This is clearly illustrated by the suppressor of cytokine signalling (SOCS) proteins which are increasingly seen as a central component of the regulation of the action of hormones and cytokines that signal through the cytokine receptor complex. The SOCS protein family is probably more extensive than currently recognised; its members may have differential tissue expression and their po

APA, Harvard, Vancouver, ISO, and other styles

27

Riedl, Isabelle, Megan E. Osler, Marie Björnholm та ін. "AMPKγ3 is dispensable for skeletal muscle hypertrophy induced by functional overload". American Journal of Physiology-Endocrinology and Metabolism 310, № 6 (2016): E461—E472. http://dx.doi.org/10.1152/ajpendo.00387.2015.

Full text

Abstract:

Mechanisms regulating skeletal muscle growth involve a balance between the activity of serine/threonine protein kinases, including the mammalian target of rapamycin (mTOR) and 5′-AMP-activated protein kinase (AMPK). The contribution of different AMPK subunits to the regulation of cell growth size remains inadequately characterized. Using AMPKγ3 mutant-overexpressing transgenic Tg-Prkag3 225Q and AMPKγ3-knockout ( Prkag3−/−) mice, we investigated the requirement for the AMPKγ3 isoform in functional overload-induced muscle hypertrophy. Although the genetic disruption of the γ3 isoform did not im

APA, Harvard, Vancouver, ISO, and other styles

28

Cano-Gauci, Danielle F., Howard H. Song, Huiling Yang, et al. "Glypican-3–Deficient Mice Exhibit Developmental Overgrowth and Some of the Abnormalities Typical of Simpson-Golabi-Behmel Syndrome." Journal of Cell Biology 146, no. 1 (1999): 255–64. http://dx.doi.org/10.1083/jcb.146.1.255.

Full text

Abstract:

Glypicans are a family of heparan sulfate proteoglycans that are linked to the cell surface through a glycosyl–phosphatidylinositol anchor. One member of this family, glypican-3 (Gpc3), is mutated in patients with the Simpson-Golabi-Behmel syndrome (SGBS). These patients display pre- and postnatal overgrowth, and a varying range of dysmorphisms. The clinical features of SGBS are very similar to the more extensively studied Beckwith-Wiedemann syndrome (BWS). Since BWS has been associated with biallelic expression of insulin-like growth factor II (IGF-II), it has been proposed that GPC3 is a neg

APA, Harvard, Vancouver, ISO, and other styles

29

Zhang, Zhao, Thomas Gallagher, Philipp E. Scherer, and Bruce Beutler. "Tissue-specific disruption ofKbtbd2uncovers adipocyte-intrinsic and -extrinsic features of theteenylipodystrophy syndrome." Proceedings of the National Academy of Sciences 117, no. 21 (2020): 11829–35. http://dx.doi.org/10.1073/pnas.2000118117.

Full text

Abstract:

Loss of KBTBD2 in all tissues causes theteenyphenotype, characterized by insulin resistance with late failure of insulin production, severe hyperglycemia/diabetes, lipodystrophy, hepatosteatosis, and growth retardation. KBTBD2 maintains insulin sensitivity in adipocytes by restricting the abundance of p85α. However, the possible physiological contribution or contributions of KBTBD2 have not yet been examined in other tissues. Here we show that mice with an adipocyte-specific knockout ofKbtbd2accumulate p85α in white and brown adipose tissues, causing insulin resistance, moderate rather than se

APA, Harvard, Vancouver, ISO, and other styles

30

Luo, Liping, Wanxiang Jiang, Hui Liu, et al. "De-silencing Grb10 contributes to acute ER stress-induced steatosis in mouse liver." Journal of Molecular Endocrinology 60, no. 4 (2018): 285–97. http://dx.doi.org/10.1530/jme-18-0018.

Full text

Abstract:

The growth factor receptor bound protein GRB10 is an imprinted gene product and a key negative regulator of the insulin, IGF1 and mTORC1 signaling pathways. GRB10 is highly expressed in mouse fetal liver but almost completely silenced in adult mice, suggesting a potential detrimental role of this protein in adult liver function. Here we show that the Grb10 gene could be reactivated in adult mouse liver by acute endoplasmic reticulum stress (ER stress) such as tunicamycin or a short-term high-fat diet (HFD) challenge, concurrently with increased unfolded protein response (UPR) and hepatosteatos

APA, Harvard, Vancouver, ISO, and other styles

31

Wilson, Rebecca L., Weston Troja, Emily K. Sumser, Alec Maupin, Kristin Lampe, and Helen N. Jones. "Insulin-like growth factor 1 signaling in the placenta requires endothelial nitric oxide synthase to support trophoblast function and normal fetal growth." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 5 (2021): R653—R662. http://dx.doi.org/10.1152/ajpregu.00250.2020.

Full text

Abstract:

Currently, there is no effective treatment for placental dysfunction in utero. In a ligated mouse model of fetal growth restriction (FGR), nanoparticle-mediated human insulin-like 1 growth factor ( hIGF1) gene delivery (NP-Plac1-hIGF1) increased hIGF1 expression and maintained fetal growth. However, whether it can restore fetal growth remains to be determined. Using the endothelial nitric oxide synthase knockout (eNOS−/−) mouse model, a genetic model of FGR, we found that despite inducing expression of hIGF1 in the placentas treated with NP-Plac1-hIGF1 ( P = 0.0425), FGR did not resolve. This

APA, Harvard, Vancouver, ISO, and other styles

32

Feng, Yuxin, Xuan Zhou, and Yi Zheng. "The Rho GTPase Cdc42 Is a Key Regulator of the Genesis and Function of Bone Marrow Derived Endothelial-Like Cells." Blood 116, no. 21 (2010): 2109. http://dx.doi.org/10.1182/blood.v116.21.2109.2109.

Full text

Abstract:

Abstract Abstract 2109 In addition to maintaining steady state hematopoiesis in the adult life, bone marrow (BM) derived cells contain endothelial progenitor cell (EPC) activity and may play a role in promoting vascular regeneration upon injury or angiogenesis during tumor progression. Whether hematopoietic stem/progenitor cells (HSPCs) in the BM can give rise to functional EPCs and if they contribute significantly to endothelial cell regeneration remain controversial questions. Cdc42 is a member of the Rho GTPase family that has been shown to play essential and unique roles in multiple lineag

APA, Harvard, Vancouver, ISO, and other styles

33

Benrick, Anna, Belén Chanclón, Peter Micallef, et al. "Adiponectin protects against development of metabolic disturbances in a PCOS mouse model." Proceedings of the National Academy of Sciences 114, no. 34 (2017): E7187—E7196. http://dx.doi.org/10.1073/pnas.1708854114.

Full text

Abstract:

Adiponectin, together with adipocyte size, is the strongest factor associated with insulin resistance in women with polycystic ovary syndrome (PCOS). This study investigates the causal relationship between adiponectin levels and metabolic and reproductive functions in PCOS. Prepubertal mice overexpressing adiponectin from adipose tissue (APNtg), adiponectin knockouts (APNko), and their wild-type (WT) littermate mice were continuously exposed to placebo or dihydrotestosterone (DHT) to induce PCOS-like traits. As expected, DHT exposure led to reproductive dysfunction, as judged by continuous ane

APA, Harvard, Vancouver, ISO, and other styles

34

Romacho, Tania, Henrike Sell, Ira Indrakusuma, et al. "DPP4 deletion in adipose tissue improves hepatic insulin sensitivity in diet-induced obesity." American Journal of Physiology-Endocrinology and Metabolism 318, no. 5 (2020): E590—E599. http://dx.doi.org/10.1152/ajpendo.00323.2019.

Full text

Abstract:

Besides a therapeutic target for type 2 diabetes, dipeptidyl peptidase 4 (DPP4) is an adipokine potentially upregulated in human obesity. We aimed to explore the role of adipocyte-derived DPP4 in diet-induced obesity and insulin resistance with an adipose tissue-specific knockout (AT-DPP4-KO) mouse. Wild-type and AT-DPP4-KO mice were fed for 24 wk with a high fat diet (HFD) and characterized for body weight, glucose tolerance, insulin sensitivity by hyperinsulinemic-euglycemic clamp, and body composition and hepatic fat content. Image and molecular biology analysis of inflammation, as well as

APA, Harvard, Vancouver, ISO, and other styles

35

Wang, Pengfei, Michael R. Bowl, Stephanie Bender, et al. "Parafibromin, a Component of the Human PAF Complex, Regulates Growth Factors and Is Required for Embryonic Development and Survival in Adult Mice." Molecular and Cellular Biology 28, no. 9 (2008): 2930–40. http://dx.doi.org/10.1128/mcb.00654-07.

Full text

Abstract:

ABSTRACT Parafibromin, a transcription factor associated with the PAF complex, is encoded by the HRPT2 gene, mutations of which cause the hyperparathyroidism-jaw tumor syndrome (OMIM145001). To elucidate the function of parafibromin, we generated conventional and conditional Hrpt2 knockout mice and found that Hrpt2 −/− mice were embryonic lethal by embryonic day 6.5 (E6.5). Controlled deletion of Hrpt2 after E8.5 resulted in apoptosis and growth retardation. Deletion of Hrpt2 in adult mice led to severe cachexia and death within 20 days. To explore the mechanism underlying the embryonic lethal

APA, Harvard, Vancouver, ISO, and other styles

36

Biniszkiewicz, Detlev, Joost Gribnau, Bernard Ramsahoye, et al. "Dnmt1 Overexpression Causes Genomic Hypermethylation, Loss of Imprinting, and Embryonic Lethality." Molecular and Cellular Biology 22, no. 7 (2002): 2124–35. http://dx.doi.org/10.1128/mcb.22.7.2124-2135.2002.

Full text

Abstract:

ABSTRACT Biallelic expression of Igf2 is frequently seen in cancers because Igf2 functions as a survival factor. In many tumors the activation of Igf2 expression has been correlated with de novo methylation of the imprinted region. We have compared the intrinsic susceptibilities of the imprinted region of Igf2 and H19, other imprinted genes, bulk genomic DNA, and repetitive retroviral sequences to Dnmt1 overexpression. At low Dnmt1 methyltransferase levels repetitive retroviral elements were methylated and silenced. The nonmethylated imprinted region of Igf2 and H19 was resistant to methylatio

APA, Harvard, Vancouver, ISO, and other styles

37

Wesolowski, Radoslaw, Elisabeth Kowenz-Leutz, Karin Zimmermann, et al. "Myeloid transformation by MLL-ENL depends strictly on C/EBP." Life Science Alliance 4, no. 1 (2020): e202000709. http://dx.doi.org/10.26508/lsa.202000709.

Full text

Abstract:

Chromosomal rearrangements of the mixed-lineage leukemia gene MLL1 are the hallmark of infant acute leukemia. The granulocyte-macrophage progenitor state forms the epigenetic basis for myelomonocytic leukemia stemness and transformation by MLL-type oncoproteins. Previously, it was shown that the establishment of murine myelomonocytic MLL-ENL transformation, but not its maintenance, depends on the transcription factor C/EBPα, suggesting an epigenetic hit-and-run mechanism of MLL-driven oncogenesis. Here, we demonstrate that compound deletion of Cebpa/Cebpb almost entirely abrogated the growth a

APA, Harvard, Vancouver, ISO, and other styles

38

Faught, Erin, and Mathilakath M. Vijayan. "Glucocorticoid and mineralocorticoid receptor activation modulates postnatal growth." Journal of Endocrinology 244, no. 2 (2020): 261–71. http://dx.doi.org/10.1530/joe-19-0358.

Full text

Abstract:

During early development, stress or exogenous glucocorticoid (GC) administration reduces body mass in vertebrates, and this is associated with the glucocorticoid receptor (GR) activation. Although GCs also activate the mineralocorticoid receptor (MR), the physiological significance of MR activation on early developmental growth is unknown. We tested the hypothesis that activation of both GR and MR are required for postnatal growth suppression by GCs. Differential regulation of GR and MR activation was achieved by using ubiquitous GR- (GRKO) and MR- (MRKO) knockout zebrafish (Danio rerio) in co

APA, Harvard, Vancouver, ISO, and other styles

39

Liu, Hong, Jian Guo, Lin Wang, et al. "Distinctive anabolic roles of 1,25-dihydroxyvitamin D3 and parathyroid hormone in teeth and mandible versus long bones." Journal of Endocrinology 203, no. 2 (2009): 203–13. http://dx.doi.org/10.1677/joe-09-0247.

Full text

Abstract:

To assess the roles of 1,25-dihydroxyvitamin D (1,25(OH)2D) and parathyroid hormone (PTH) in hard tissue formation in oro-facial tissues, we examined the effect of either 1,25(OH)2D or PTH deficiency on dentin and dental alveolar bone formation and mineralization in the mandibles, and osteoblastic bone formation in long bones of 1α-hydroxylase knockout (1α(OH)ase−/−) mice. Compared with wild-type mice, the mineral density was decreased in the teeth and mandibles, and unmineralized dentin (predentin and biglycan immunopositive dentin) and unmineralized bone matrix in the dental alveolar bone we

APA, Harvard, Vancouver, ISO, and other styles

40

Nölting, Svenja, Edwin Garcia, Ghassan Alusi, et al. "Combined blockade of signalling pathways shows marked anti-tumour potential in phaeochromocytoma cell lines." Journal of Molecular Endocrinology 49, no. 2 (2012): 79–96. http://dx.doi.org/10.1530/jme-12-0028.

Full text

Abstract:

Currently, there is no completely effective therapy available for metastatic phaeochromocytomas (PCCs) and paragangliomas. In this study, we explore new molecular targeted therapies for these tumours, using one more benign (mouse phaeochromocytoma cell (MPC)) and one more malignant (mouse tumour tissue (MTT)) mouse PCC cell line – both generated from heterozygous neurofibromin 1 knockout mice. Several PCC-promoting gene mutations have been associated with aberrant activation of PI3K/AKT, mTORC1 and RAS/RAF/ERK signalling. We therefore investigated different agents that interfere specifically w

APA, Harvard, Vancouver, ISO, and other styles

41

Pharaoh, Gavin, Daniel Owen, Alexander Yeganeh, et al. "Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function." Molecular Neurobiology 57, no. 3 (2019): 1317–31. http://dx.doi.org/10.1007/s12035-019-01821-4.

Full text

Abstract:

AbstractAge-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1

APA, Harvard, Vancouver, ISO, and other styles

42

Lepa, Carolin, Sascha Hoppe, Antje Stöber, et al. "TrkC Is Essential for Nephron Function and Trans-Activates Igf1R Signaling." Journal of the American Society of Nephrology, December 30, 2020, ASN.2020040424. http://dx.doi.org/10.1681/asn.2020040424.

Full text

Abstract:

BackgroundInjury to kidney podocytes often results in chronic glomerular disease and consecutive nephron malfunction. For most glomerular diseases, targeted therapies are lacking. Thus, it is important to identify novel signaling pathways contributing to glomerular disease. Neurotrophic tyrosine kinase receptor 3 (TrkC) is expressed in podocytes and the protein transmits signals to the podocyte actin cytoskeleton.MethodsNephron-specific TrkC knockout (TrkC-KO) and nephron-specific TrkC-overexpressing (TrkC-OE) mice were generated to dissect the role of TrkC in nephron development and maintenan

APA, Harvard, Vancouver, ISO, and other styles

43

Higashi, Yusuke, Shaw-yung Shai, Sergiy Sukhanov, Catherine Kim, and Patrice Delafontaine. "Abstract 464: Knockout of Insulin-like Growth Factor-1 Receptor in Monocyte/Macrophage Promotes Atherosclerosis and Induces an Unstable Plaque Phenotype." Arteriosclerosis, Thrombosis, and Vascular Biology 33, suppl_1 (2013). http://dx.doi.org/10.1161/atvb.33.suppl_1.a464.

Full text

Abstract:

We have previously shown that infusion of insulin-like growth factor-1 (IGF-1) exerts anti-inflammatory and anti-oxidant effects and reduces atherosclerotic burden in apolipoprotein E deficient (Apoe-/-) mice. Monocytes/macrophages play a pivotal role in atherogenesis and express high levels of IGF-1 receptor (IGF-1R); however the potential effects of IGF-1 on their function are unknown. Thus, we created monocyte/macrophage specific IGF-1R knockout mice (MΦIgf1rKO) by crossing Igf1r floxed mice with Lysozyme-Cre mice, both on Apoe-/- background, and evaluated atherosclerosis by feeding a high

APA, Harvard, Vancouver, ISO, and other styles

44

Holzenberger, M. "The GH/IGF-I axis and longevity." European Journal of Endocrinology, August 1, 2004, S23—S27. http://dx.doi.org/10.1530/eje.0.151s023.

Full text

Abstract:

Several converging lines of evidence obtained over the last years in a wide variety of experimental model organisms suggest that the ageing process is regulated by genes that encode proteins from the somatotroph axis: longevity genes like daf-2, which were identified using mutant Caenorhabditis elegans strains, turned out to be orthologues of the mammalian genes encoding insulin-like signalling cascade proteins. Transgenic flies with mutations in the corresponding insect genes showed a similar pattern of increased lifespan. Finally, mice with spontaneous mutations leading to pituitary hormone

APA, Harvard, Vancouver, ISO, and other styles

45

Cao, Congcong, Peng Duan, Wencun Li, et al. "Lack of miR-379/miR-544 Cluster Resists High-Fat Diet-Induced Obesity and Prevents Hepatic Triglyceride Accumulation in Mice." Frontiers in Cell and Developmental Biology 9 (August 30, 2021). http://dx.doi.org/10.3389/fcell.2021.720900.

Full text

Abstract:

Non-alcoholic fatty liver disease (NAFLD) affects obesity-associated metabolic syndrome, which exhibits hepatic steatosis, insulin insensitivity and glucose intolerance. Emerging evidence suggests that microRNAs (miRNAs) are essential for the metabolic homeostasis of liver tissues. Many hepatic miRNAs located in the miR-379/miR-544 cluster were significantly increased in leptin-receptor-deficient type 2 mice (db/db), a mouse model of diabetes. However, the function of the miR-379/miR-544 cluster in the process of hepatic steatosis remains unclear. Here, we report that the novel function of miR

APA, Harvard, Vancouver, ISO, and other styles

46

Sidhom, Silvana, Augusto Schneider, Yimin Fang та ін. "17α-Estradiol Modulates IGF1 and Hepatic Gene Expression in a Sex-Specific Manner". Journals of Gerontology: Series A, 28 серпня 2020. http://dx.doi.org/10.1093/gerona/glaa215.

Full text

Abstract:

Abstract Aging is the greatest risk factor for most chronic diseases. The somatotropic axis is one of the most conserved biological pathways that regulates aging across species. 17α-Estradiol (17α-E2), a diastereomer of 17β-estradiol (17β-E2), was recently found to elicit health benefits, including improved insulin sensitivity and extend longevity exclusively in male mice. Given that 17β-E2 is known to modulate somatotropic signaling in females through actions in the pituitary and liver, we hypothesized that 17α-E2 may be modulating the somatotropic axis in males, thereby contributing to healt

APA, Harvard, Vancouver, ISO, and other styles

47

Sarmento-Cabral, Andre, Mercedes del Rio-Moreno, Mari C. Vazquez-Borrego, et al. "SUN-LB52 The Protective Effects of Hepatocyte GH Receptor (GHR) Signaling Against Steatosis and Liver Injury Is Sexually Dimorphic and Autonomous of IGF1." Journal of the Endocrine Society 4, Supplement_1 (2020). http://dx.doi.org/10.1210/jendso/bvaa046.2287.

Full text

Abstract:

Abstract GH dysregulation contributes to the development of non-alcoholic fatty liver disease (NAFLD), however debate remains as to the relative contribution of the direct vs indirect effects of GH, via IGF1. Mouse models with congenital, liver-specific knockout of the GHR, JAK2 or STAT5, as adults exhibit steatosis, glucose intolerance, insulin resistance and white adipose tissue (WAT) lipolysis. It is believed that fatty liver is due to the dramatic reduction in circulating IGF1 altering systemic metabolism, due to loss of the insulin-like effects of IGF1 and the loss of IGF1 negative feedba

APA, Harvard, Vancouver, ISO, and other styles

48

Eddiry, Sanaa, Gwenaelle Diene, Catherine Molinas, et al. "SNORD116 and growth hormone therapy impact IGFBP7 in Prader–Willi syndrome." Genetics in Medicine, May 26, 2021. http://dx.doi.org/10.1038/s41436-021-01185-y.

Full text

Abstract:

Abstract Purpose Prader–Willi syndrome (PWS) is a neurodevelopmental disorder with hypothalamic dysfunction due to deficiency of imprinted genes located on the 15q11-q13 chromosome. Among them, the SNORD116 gene appears critical for the expression of the PWS phenotype. We aimed to clarify the role of SNORD116 in cellular and animal models with regard to growth hormone therapy (GHT), the main approved treatment for PWS. Methods We collected serum and induced pluripotent stem cells (iPSCs) from GH-treated PWS patients to differentiate into dopaminergic neurons, and in parallel used a Snord116 kn

APA, Harvard, Vancouver, ISO, and other styles

49

Li, Zhongchi, Kang Xu, Yannan Guo, et al. "A high‐fat diet reverses metabolic disorders and premature aging by modulating insulin and IGF1 signaling in SIRT6 knockout mice." Aging Cell 19, no. 3 (2020). http://dx.doi.org/10.1111/acel.13104.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Grundmann, Sarah M., Alexandra Schutkowski, Christian Berger, Anja C. Baur, Bettina König, and Gabriele I. Stangl. "High-phosphorus diets reduce aortic lesions and cardiomyocyte size and modify lipid metabolism in Ldl receptor knockout mice." Scientific Reports 10, no. 1 (2020). http://dx.doi.org/10.1038/s41598-020-77509-w.

Full text

Abstract:

AbstractThe consumption of phosphorus in Western populations largely exceeds the recommended intake, while vitamin D supply is often insufficient. Both situations are linked to an increased cardiovascular risk. A 17-week two-factorial study with Ldl receptor-/- mice was conducted to investigate the cardiovascular impact of dietary phosphorus [adequate (0.3%; P0.3) vs. high (1.5%; P1.5)] in combination with a low (50 IU/kg; D50) or adequate vitamin D diet (1000 IU/kg; D1000). The data demonstrate that mice fed the P1.5 vs. P0.3 diets developed smaller vascular lesions (p = 0.013) and cardiac hy

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!