Results 101 to 110 of about 9,698 (210)

Abstracts

open access: yesMolecular Oncology, Volume 20, Issue S1, Page 1-692, August 2026.
Abstracts submitted to the ‘EACR 2026 Congress: Innovative Cancer Science’, from 08–11 June 2026 and accepted by the Congress Organising Committee are published in this Supplement of Molecular Oncology, an affiliated journal of the European Association for Cancer Research (EACR).
wiley   +1 more source

The p75NTR intracellular domain generated by neurotrophin-induced receptor cleavage potentiates Trk signaling

open access: yes, 2010
The p75 neurotrophin receptor (p75NTR) potentiates Trk signaling, but the underlying mechanisms remain uncertain. Here, we examine the relationship between p75NTR cleavage and Trk signaling. We found that, in PC12 cells, nerve growth factor (NGF) induces
Xiaoyang Liu   +7 more
core   +1 more source

p75NTR+ Cardiac Macrophages Exacerbate Adverse Remodeling after Myocardial Infarction

open access: yes
​Background: The subacute phase of myocardial infarction (MI) is a critical window for cardiac repair, but the mechanisms governing extracellular matrix (ECM) remodelling during this period remain unclear.
Ru-Yi Luo   +11 more
core   +1 more source

Human p75NTR extracellular domain (p75NTRECD) was detected in urine of humans living with ALS by immuno-precipitation/western blot.

open access: yes, 2014
Human p75NTRECD was detected after immuno-precipitation (IP) of 500 µg urinary protein from ALS patients 1 and 2 (lane 4, lane 6) but not from healthy controls A and B (lane 5, lane 7).
Mary-Louise Rogers (514681)   +4 more
core   +1 more source

p75NTR antibody-conjugated microspheres: an approach to guided tissue regeneration by selective recruitment of endogenous periodontal ligament cells

open access: yesFrontiers in Bioengineering and Biotechnology
Repairing defects in alveolar bone is essential for regenerating periodontal tissue, but it is a formidable challenge. One promising therapeutic approach involves using a strategy that specifically recruits periodontal ligament cells (PDLCs) with high ...
Xuqiang Zou   +10 more
doaj   +1 more source

Structure of the C-terminal domain of TRADD reveals a novel fold in the death domain superfamily

open access: yesScientific Reports, 2017
The TNFR1-associated death domain protein (TRADD) is an intracellular adaptor protein involved in various signaling pathways, such as antiapoptosis. Its C-terminal death domain (DD) is responsible for binding other DD-containing proteins including the ...
Ning Zhang   +3 more
doaj   +1 more source

Signaling of the neurotrophin receptor p75NTR in breast cancer cells

open access: yes, 2010
Les données accumulées par notre laboratoire montrent une action pro-tumorale des neurotrophines dans le cancer du sein via notamment des effets anti-apoptotiques du NGF, du BDNF et de la NT4/5.
Verbeke, Stéphanie
core  

Protomic analysis of the receptor p75NTR in breast cancer

open access: yes, 2011
Le facteur de croissance neurotrophique NGF (Nerve Growth Factor) est un facteur mitogène et de survie pour les cellules de cancer du sein alors qu’il est sans effet sur la croissance des cellules épithéliales mammaires normales. Ce facteur de croissance
Wilmet, Jean-Philippe
core  

p75NTR is involved in inflammatory responses in psoriasis

open access: yes, 2023
Background. Psoriasis is a cutaneous chronic inflammatory disease, characterized by excessive proliferation and abnormal differentiation of keratinocytes and infiltration of multiple inflammatory cells. Moreover, different neuropeptides have been involved in the pathogenesis of psoriasis. NGF is known to increase in psoriasis and to cause neuropeptides
Alessandra Magenta   +8 more
openaire   +1 more source

Analysis of cell surface receptor expression on hepatocytes or HSCs and NGFp binding specificity to p75NTR.

open access: yes, 2013
(A) Fluorescence microscopic images of p75NTR expression (red) on primary hepatocytes and HSCs (DAPI stained nuclei are blue) showing a HSC-specific expression of p75NTR (10x).
Ottmar Herchenröder (204013)   +8 more
core   +1 more source

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