نتایج جستجو برای: btk expression

تعداد نتایج: 873168  

Journal: :iranian journal of immunology 0
asghar aghamohammadi department of clinical pediatric immunology, children's medical center hospital, tehran university of medical sciences, tehran, iran ali akbar amirzargar department of immunogenetics, tehran university of medical sciences, tehran, iran nima parvaneh department of clinical pediatric immunology, children's medical center hospital, tehran university of medical sciences, tehran, iran paul marjousef department of immunogenetics, tehran university of medical sciences, tehran, iran mostafa moin department of clinical pediatric immunology, children's medical center hospital, tehran university of medical sciences, tehran, iran abdolhassan farhoudi department of clinical pediatric immunology, children's medical center hospital, tehran university of medical sciences, tehran, iran mehdi yeganeh

background: the b-cell defect in x-linked agammaglobulinemia (xla) is caused by mutations in the gene for bruton's tyrosine kinase (btk). btk mutations result in deficient expression of btk protein in peripheral blood monocytes. methods: using the anti-btk monoclonal antibody (48-2h), a flow cytometric analysis of intra cytoplasmic btk protein expression in monocytes was performed to ident...

Abdolhassan Farhoudi Ali Akbar Amirzargar, Asghar Aghamohammadi, Mehdi Yeganeh Mostafa Moin Nima Parvaneh Paul Marjousef Toshio Miyawaki

Background: The B-cell defect in X-linked agammaglobulinemia (XLA) is caused by mutations in the gene for Bruton's tyrosine kinase (BTK). BTK mutations result in deficient expression of BTK protein in peripheral blood monocytes. Methods: Using the anti-BTK monoclonal antibody (48-2H), a flow cytometric analysis of intra cytoplasmic BTK protein expression in monocytes was performed to identify I...

آقا محمدی, اصغر, رضایی, نیما, سروری زنجانی, رحیم, معین, مصطفی, ناصری, سعید, پروانه, نیما, پور پاک, زهرا,

Correlation of Null Btk Expression and Gene Noncoding Mutations in XLA Patients Nasseri S1, Sorouri R2, Pourpak Z3, Rezaei N4, Moin M5, Parvaneh N6, Aghamohammadi A7 1 Dept of Molecular Biology, Immunology, Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran 2 Baqiyatallah University of Medical Sciences, Tehran, Iran and, Zanjan University of Medical Scien...

Journal: :Blood 1998
T Futatani T Miyawaki S Tsukada S Hashimoto T Kunikata S Arai M Kurimoto Y Niida H Matsuoka Y Sakiyama T Iwata S Tsuchiya O Tatsuzawa K Yoshizaki T Kishimoto

The B-cell defect in X-linked agammaglobulinemia (XLA) is caused by mutations in the gene for Bruton's tyrosine kinase (BTK). Using the anti-BTK monoclonal antibody (48-2H), a flow cytometric analysis of intracytoplasmic BTK protein expressed in monocytes was successfully performed. To examine the possible identification of XLA patients and female carriers by this assay, we studied 41 unrelated...

2017
Chunyan Gu Hailin Peng Yue Lu Hongbao Yang Zhidan Tian Gang Yin Wen Zhang Sicheng Lu Yi Zhang Ye Yang

We previously explored the role of BTK in maintaining multiple myeloma stem cells (MMSCs) self-renewal and drug-resistance. Here we investigated the elevation of BTK suppressing MM cellular senescence, a state of irreversible cellular growth arrest. We firstly discovered that an increased expression of BTK in MM samples compared to normal controls by immunohistochemistry (IHC), and significant ...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2002
David A Fruman Gregory Z Ferl Sam S An Amber C Donahue Anne B Satterthwaite Owen N Witte

Bruton's tyrosine kinase (Btk) acts downstream of phosphoinositide 3-kinase (PI3K) in a pathway required for B cell receptor (BCR)-dependent proliferation. We used DNA microarrays to determine what fraction of genes this pathway influences and to investigate whether PI3K and Btk mediate distinct gene regulation events. As complete loss-of-function mutations in PI3K and Btk alter B cell subpopul...

2016
Li Wei Yu-Kai Su Chien-Min Lin Tsu-Yi Chao Shang-Pen Huang Thanh-Tuan Huynh Hsun-Jin Jan Jacqueline Whang-Peng Jeng-Fong Chiou Alexander T.H. Wu Michael Hsiao

Standard interventions for glioma include surgery, radiation and chemotherapies but the prognosis for malignant cases such as glioblastoma multiforme remain grim. Even with targeted therapeutic agent, bevacitumab, malignant glioma often develops resistance and recurrence. Thus, developing alternative interventions (therapeutic targets, biomarkers) is urgently required. Bruton's tyrosine kinase ...

2015
Marcelo A Teocchi Vanessa Domingues Ramalho Beatriz M Abramczuk Lília D'Souza-Li Maria Marluce Santos Vilela

Mutations in the Bruton agammaglobulinemia tyrosine kinase (BTK) gene are responsible for X-linked agammaglobulinemia (XLA). Unfolded or misfolded proteins can trigger stress pathways in the endoplasmic reticulum (ER), known as unfolded protein response (UPR). The aim was to clarify the involvement of UPR in XLA pathophysiology. By reverse transcription-quantitative PCR, we evaluated the expres...

Journal: :The Journal of clinical investigation 2014
Burcu Bestas Pedro M D Moreno K Emelie M Blomberg Dara K Mohammad Amer F Saleh Tolga Sutlu Joel Z Nordin Peter Guterstam Manuela O Gustafsson Shabnam Kharazi Barbara Piątosa Thomas C Roberts Mark A Behlke Matthew J A Wood Michael J Gait Karin E Lundin Samir El Andaloussi Robert Månsson Anna Berglöf Jesper Wengel C I Edvard Smith

X-linked agammaglobulinemia (XLA) is an inherited immunodeficiency that results from mutations within the gene encoding Bruton's tyrosine kinase (BTK). Many XLA-associated mutations affect splicing of BTK pre-mRNA and severely impair B cell development. Here, we assessed the potential of antisense, splice-correcting oligonucleotides (SCOs) targeting mutated BTK transcripts for treating XLA. Bot...

Journal: :The EMBO journal 1998
A C Fluckiger Z Li R M Kato M I Wahl H D Ochs R Longnecker J P Kinet O N Witte A M Scharenberg D J Rawlings

Bruton's tyrosine kinase (Btk) is essential for B-lineage development and represents an emerging family of non-receptor tyrosine kinases implicated in signal transduction events initiated by a range of cell surface receptors. Increased dosage of Btk in normal B cells resulted in a striking enhancement of extracellular calcium influx following B-cell antigen receptor (BCR) cross-linking. Ectopic...

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