Results 51 to 60 of about 13,071,502 (301)

From mice to humans—divergent strategies for intestinal homeostasis and regeneration

FEBS Letters, EarlyView.
Recent advances such as organoid genome editing, xenotransplantation, imaging, and whole‐genome sequencing have enabled direct studies of human intestinal stem cells (ISCs). These studies reveal species‐specific features, including slower ISC proliferation, distinct injury responses, slower somatic mutation accumulation in humans, and an inverse ...
Keiko Ishikawa, Shinya Sugimoto, Toshiro Sato   +2 more
wiley   +1 more source

Associations among IGF-1, IGF2, IGF-1R, IGF-2R, IGFBP-3, insulin genetic polymorphisms and central precocious puberty in girls

BMC Endocrine Disorders, 2018
Background Insulin and insulin-like growth factor (IGF)-1 coupled with growth hormone helps control timing of sexual maturation. Mutations and variants in multiple genes are associated with development or reduced risk of central precocious puberty (CPP).
Hua-Pin Chang, Shun-Fa Yang, Shu-Li Wang, Pen-Hua Su   +3 more
doaj   +1 more source

Discerning protein pools by selective staining with self‐labeling tags

FEBS Letters, EarlyView.
Cell surface proteins have an intra‐ and extracellular pool. Combining genetic fusion to self‐labeling tags that can be addressed with small molecule fluorophores allows separating these pools. We highlight recent developments and techniques for state‐of‐the‐art interrogation of cell surface proteins in the complex tissue setting.
Kati Fischermanns, Johannes Broichhagen
wiley   +1 more source

Insulin-Like Growth Factors and the Brain [PDF]

Endocrinology, 2008
The IGFs have interested biologists and physicians for many decades; starting with the somatomedin hypothesis as presented by Daughaday and Salmon in 1957 (1). It was initially thought that somatomedin C (IGF-I) was the liver-derived, circulating form of IGF and controlled postnatal growth in response to GH. After the advent of molecular endocrinology,
openaire   +2 more sources

Nutrient/TOR signaling controls adipose mitochondrial transcription factor A (TFAM) to regulate organismal growth in Drosophila

FEBS Letters, EarlyView.
Animals must match their growth rate to available nutrients. We show that in Drosophila larvae, the nutrient‐sensing TOR kinase controls growth by regulating levels of TFAM, a key regulator of mitochondrial function, in the adipose tissue. When nutrients are abundant, high TOR activity suppresses TFAM, lowering mitochondrial bioenergetic activity and ...
Shrivani Sriskanthadevan‐Pirahas, Shahoon Khan, Abhishek Sharma, Byoungchun Lee, Savraj S. Grewal   +4 more
wiley   +1 more source

Autophagy and mitophagy in pancreatic β‐cell homeostasis and their involvement in diabetes pathophysiology

FEBS Letters, EarlyView.
This review focuses on the role of autophagy and mitophagy in maintaining pancreatic β‐cell function and homeostasis. We discuss how genetic defects affecting these pathways contribute to the development of type 1, type 2, monogenic, and gestational diabetes. We further explore their potential as therapeutic targets. Created in BioRender.
Yunkyeong Lee, Mingming Tong, Anna L. Gloyn   +2 more
wiley   +1 more source

Growth Hormone, Insulin-Like Growth Factors, and the Skeleton [PDF]

Endocrine Reviews, 2008
GH and IGF-I are important regulators of bone homeostasis and are central to the achievement of normal longitudinal bone growth and bone mass. Although GH may act directly on skeletal cells, most of its effects are mediated by IGF-I, which is present in the systemic circulation and is synthesized by peripheral tissues.
GIUSTINA, Andrea, MAZZIOTTI, Gherardo, CANALIS E.   +2 more
openaire   +4 more sources

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

Molecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

Glucokinase links Kruppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease [PDF]

, 2011
The polymorphism, KLF6-IVS1-27A, in the Krüppel-like factor 6 (KLF6) transcription factor gene enhances its splicing into antagonistic isoforms and is associated with delayed histological progression of nonalcoholic fatty liver disease (NAFLD).
Gastaldelli, Amalia, Lee, Y., Isabel Fiel, Elisabetta Bugianesi, Miele, L., Lee, U., Bugianesi, E., Emma Buzzigoli, Andrea Mari, Pascoe, L., Mark Walker, Christopher P. Day, Burt, Alastair D., Walker, M., Bechmann, L., Hui, Kei Y, Fiel, I., Buzzigoli, E., Bechmann, Lars P., Miele, Luca, Fiel, Isabel., Luca Miele, Mari, Andrea, Patman, G., Ursula Muñoz, Day, Christopher P., Vetter, Diana., Burt, A., Lee, Young-Min., Munoz, Ursula., Hannivoort, Rebekka A., Alastair D. Burt, Amalia Gastaldelli, Walker, Mark., Agius, Loranne, Mari, A., Agius, Loranne., et al., Buzzigoli, Emma, Walker, Mark, Loranne Agius, Scott L. Friedman, Lee, Young-Min, Pascoe, Laura., Miele, Luca., Munoz, Ursula, Hui, K., Day, C., Laura Pascoe, Pascoe, Laura, Gastaldelli, Amalia., Fiel, Isabel, Ursula E. Lee, Gillian L. Patman, Munoz, U., Kei Y. Hui, Agius, L., Mari, Andrea., Vetter, D., Demetrio Ciociaro, Ciociaro, D., Buzzigoli, Emma., Lars P. Bechmann, Helen L. Reeves, Patman, Gillian L., Hannivoort, Rebekka A ., Ciociaro, Demetrio, Ciociaro, Demetrio., Mu?oz, Ursula, Bugianesi, Elisabetta, Diana Vetter, Reeves, Helen L., Hannivoort, R., Lee, Ursula E., Rebekka A. Hannivoort, Bugianesi, Elisabetta., Young-Min Lee, Vetter, Diana, Hui, Kei Y., Friedman, Scott L., Gastaldelli, A.   +80 more
core   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source