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Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
In parallel with the invagination of the oral ectoderm, pituitary precursor cells proliferate and migrate. The Wnt and Shh pathways regulate proliferation, while the Bmp and Fgf pathways participate in both proliferation and cellular migration. The formation of Rathke’s pouch is complete at E10.5, and the pituitary precursor cells start expressing specific factors that determine their patterns of differentiation. Activation of distinct target genes occurs in response to an established dorsal–ventral gradient of Fgf8 and a ventral–dorsal gradient of Bmp2. Thus, depending on its location, each cell has a distinct starting point within the differentiation process (Figure 5.8A). For example, ventral cells express the transcription factors Isl1 and Gata2, while the dorsal cells express Pax6, Tpit and Prop1.
Bladder exstrophy: Considerations and management of the newborn patient
Published in Prem Puri, Newborn Surgery, 2017
Peter P. Stuhldreher, John P. Gearhart
Historically, the genetics of bladder exstrophy were unknown, but recent progress using genome-wide association studies have led to a possible target gene responsible for CBE. The ISL1 gene encodes an insulin gene enhancer protein, a LIM zinc-binding/homeobox-domain transcription factor.14 Murine models of this gene have shown its role in multiple developing tissues.14 The pattern of inheritance of ISL1 is neither recessive nor purely dominant.14 Further work into clarifying and validating ISL1 is ongoing.
Clinical staging of lymphedema: How practical is it for clinical management of primary lymphedema?
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
Sandro Michelini, Alessandro Fiorentino, Alessandro Failla, Giovanni Moneta
Primary lymphedema has different clinical stages of evolution, in part mutually reversible, that influence affected patients differently from the physical, emotional, and psychological points of view. Achieving common acceptance of stages of lymphedema, as in other diseases, seems to be a problem that cannot be postponed further for reasons of “scientific communication” and for the undoubted legal medical and social impact. In more advanced clinical stages, the condition takes on the characteristics of a real “social disease” with costs generated both from medical care and from loss of productive capacity. The clinical staging, reported in the Consensus Document of the ISL,1 currently includes four clinical stages (Table 46.1); it initially included three clinical stages (I, II, and III) but recently highlighted the importance of including the “subclinical” aspect of primary lymphedema, potentially progressive (e.g., subject with blood relation with patient suffering from primary lymphedema), and the subclinical stage (stage 0) was included. Stage 0 refers to a latent or subclinical condition, where swelling is not evident despite impaired lymph transport. Stage I represents an early accumulation of fluid, relatively high in protein content, that subsides with limb elevation. Pitting may occur. Stage II signifies that limb elevation alone rarely reduces tissue swelling; pitting is manifested. Stage III encompasses lymphostatic elephantiasis where pitting is absent and trophic skin changes, such as acanthosis, fat deposits, and warty overgrowths, develop. The severity of the stages is based on the volume differences: minimal (<20% increase), moderate (20%–40% increase), and severe (>40% increase). These stages refer only to the physical condition of the extremities.
LDB1-mediated transcriptional complexes are sensitive to islet stress
Published in Islets, 2022
Yanping Liu, Jessica D. Kepple, Anath Shalev, Chad S. Hunter
Our lab and others have shown that the LIM-homeodomain transcription factor, Islet-1 (ISL1), and interacting co-regulator, LIM domain-binding protein 1 (LDB1), are required for β-cell development and function.17–20 Comparative tissue- and cell-type-specific knockout mouse models revealed that LDB1:ISL1-containing complexes are necessary for β-cell development, identity, survival, and insulin secretory function via direct regulation of several key β-cell gene targets, including MafA, Pdx1, Slc2a2, Glp1r, among others.17–20 Previously published work from our lab utilizing in vitro protein interaction screens revealed the Single-Stranded DNA-Binding protein 3 (SSBP3, also called SSDP121,22) co-regulator participates in β-cell LDB1:ISL1 complexes and contributes to the regulation of MafA expression in β-cells.23 Further, ISL1 and LDB1 are maintained in human islets,19,20 highlighting the conservation and importance of these factors to mammalian β-cells and glucose homeostasis. However, little is known of whether the expression and/or interactions of ISL1 and LDB1 are modulated by β-cell stimuli or stressors.
Surface markers of human embryonic stem cells: a meta analysis of membrane proteomics reports
Published in Expert Review of Proteomics, 2018
Faezeh Shekari, Chia-Li Han, Jaesuk Lee, Mehdi Mirzaei, Vivek Gupta, Paul A. Haynes, Bonghee Lee, Hossein Baharvand, Yu-Ju Chen, Ghasem Hosseini Salekdeh
Major breakthroughs in hESC research have been made by the identification of proteins such as cell-surface CD molecules. Ghazizadeh et al. used comparative proteomics to identify a surface marker that enabled the isolation of LIM-homeodomain transcription factor ISL1 (ISL1+) progenitor cells. ISL1 marks multipotent cardiac progenitors that give rise to cardiac muscle, endothelium, and smooth muscle cells. Using a genetic selection strategy, they enriched ISL1+ cells derived from hESCs and performed comparative quantitative proteomic analysis of enriched ISL1+ cells. They identified ALCAM (CD166) as a surface marker that enabled the isolation of ISL1+ progenitor cells. Transplantation of ALCAM+ progenitors to a rat model of myocardial infarction enhanced tissue recovery, restored cardiac function, and improved angiogenesis [40].
Heart failure risk estimation based on novel biomarkers
Published in Expert Review of Molecular Diagnostics, 2021
Feven Ataklte, Ramachandran S. Vasan
Two recent studies Xu et al. 2018 and Di et al 2020 explored the genetic basis of dilated cardiomyopathy (DCM). [113,114] Xu et al identified a novel heterozygous ISL1 mutationin a family with DCM. The study team later sequenced ISL1 in 216 unrelated patients with DCM. The ISL1 mutation, NM_002202.2: c.631A>T; p.(Lys211*) co-segregated with DCM in the family, but was absent in unrelated controls, or in Genome population databases. ISL1 gene encodes a transcription factor protein that is involved in cardiac development and remodeling. The mutant ISL1 protein lost transcriptional activity. The findings of the study may play a role in genetic counseling of patients with familial DCM [113].