Results 51 to 60 of about 182,508 (303)

Bax ablation rescues chondrocytes.

open access: yes, 2012
Proliferative HCS chondrocytic cells treated with Dexa (25 µM) for 72 hrs were analyzed for the expression of the (A) Bax and (B) Bcl-2 proteins. (C) Bax ablation protected proliferative chondrocytes from Dexa-induced apoptosis.
Lars Sävendahl (114293)   +4 more
core   +1 more source

LC3B Mediated SETDB1‐Accounted Alcoholic Steatohepatitis via Lipidation‐Dependent LAP and Lipidation‐Independent Nuclear Stabilization

open access: yesAdvanced Science, EarlyView.
SETDB1 is progressively downregulated in ALD, correlating with disease severity. SETDB1 deficiency impairs LAP by disrupting Rubicon membrane localization, leading to defective lipid droplet clearance. Concurrently, loss of SETDB1 reduces nuclear LC3B, causing R‐loop accumulation and cGAS‐STING‐driven inflammation. Lipidated LC3B mediates LAP‐dependent
Yi Zhang   +17 more
wiley   +1 more source

Elucidating the mechanism of anti-apoptotic activity of α-crystallin and its therapeutic potential [PDF]

open access: yesJournal of Stress Physiology & Biochemistry
α- Crystallins are the structural proteins of the eye lens which possess anti-apoptotic activity. Both αA- and αB- crystallins are distinct antiapoptotic regulators which can interact with Bax and Bcl-XS, proapoptotic members of the Bcl-2 family in order
Aparajita Chakraborty   +2 more
doaj  

Decoding IGLL5 Mutation‐Mediated BCR Signaling: A Novel Mechanism of CD8+ T Cell Exhaustion and Ocular MALT Lymphoma Progression

open access: yesAdvanced Science, EarlyView.
OAML harbors recurrent IGLL5 mutations that reinforce CD79A/CD79B‐associated BCR signaling. Mechanistic analysis of the S47G and A54G variants reveals induction of CXCL10/CXCL11, enhanced CD8+ T‐cell recruitment, and exhaustion‐associated dysfunction, supporting an immune‐tolerant niche.
Andi Zhao   +12 more
wiley   +1 more source

脑缺血再灌注糖尿病大鼠海马CA1区凋亡基因的表达

open access: yesZhongguo shiyan zhenduanxue, 2007
目的观察凋亡基因Bcl-2、Bax在糖尿病大鼠脑缺血再灌注海马CA1区神经元损伤中的表达。方法采用链脲佐菌素(STZ)诱导和线栓法制备糖尿病大脑中动脉闭塞模型(MCAO),应用HE染色和免疫组化方法比较糖尿病脑缺血再灌注组与缺血再灌注组海马CA1区神经元缺失、凋亡基因Bcl-2、Bax的表达。结果糖尿病脑缺血再灌注组海马CA1区神经元缺失,明显高于缺血再灌注组 ...
张季声   +7 more
doaj  

Immunohistochemical localization for Bax.

open access: yes, 2013
There was few specific expression of Bax in normal tissue (B). Protein expression of Bax was significantly increased in the epithelial cell, intestine glands and in the inflammatory cells infiltrating in the tissue of model animals (C). Treatment of SASP
Jian Ming Wang (344506), Xin Liu (43569)
core   +1 more source

Bad expression influences time to androgen escape in prostate cancer [PDF]

open access: yes, 2007
<b>OBJECTIVE</b>: To assess the role of selected downstream Bcl-2 family members (Bad, Bax, Bcl-2 and Bcl-xL) in the development of androgen-independent prostate cancer (AIPC), as androgen-deprivation therapy is the treatment of choice in ...
Teo, K.   +4 more
core   +1 more source

HNRNPD Induces Radioresistance in Nasopharyngeal Carcinoma by Sequestering GRAMD4 mRNA in Stress Granules

open access: yesAdvanced Science, EarlyView.
HNRNPD promotes radioresistance in nasopharyngeal carcinoma by enhancing stress granule assembly and sequestering GRAMD4 mRNA. This suppresses GRAMD4 translation and inhibits mitochondrial apoptosis. Targeting the integrated stress response with ISRIB restores GRAMD4 expression and sensitizes tumors to radiotherapy, revealing a translational control ...
Yingzi Li   +13 more
wiley   +1 more source

Disruption of the SNRPF–DDX24–E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression

open access: yesAdvanced Science, EarlyView.
This study identifies SNRPF as a critical oncogenic driver in ovarian cancer. By regulating a self‐sustaining SNRPF–DDX24–E2F4 feedback loop through intron retention and nonsense‐mediated decay, SNRPF couples RNA splicing with transcriptional regulation to promote tumor progression.
Yingwei Li   +4 more
wiley   +1 more source

BIN1 and ALDH1B1 Deficiency in Colonic Smooth Muscle Drives Mitochondrial Dysfunction and Fibrosis in Slow‐Transit Constipation

open access: yesAdvanced Science, EarlyView.
Slow‐transit constipation (STC) is a disabling motility disorder with unclear smooth‐muscle mechanisms. Spatial proteomic analysis of STC patient colon reveals both the central pathogenic role of smooth muscle cells (SMCs) in STC and novel regulators of intestinal motility, BIN1 and ALDH1B1.
Jianbo Liu   +10 more
wiley   +1 more source

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