Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

15.5K
The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
15.5K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

7.0K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.0K
Diversity in Cell Signaling Responses01:22

Diversity in Cell Signaling Responses

7.4K
The physiological function of a cell and cellular communication are outcomes of a range of extrinsic signals, intracellular signaling pathways, and cellular responses. No two cell types express the same repertoire of signaling components. Receptors are highly selective for their cognate ligands, but once activated, they can alter multiple cellular processes such as DNA transcription, protein synthesis, and metabolic activity. 
Graded and Abrupt Responses
Some signaling systems generate...
7.4K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

7.9K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.9K
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

14.3K
T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
14.3K
Cells of the Adaptive Immune Response01:23

Cells of the Adaptive Immune Response

8.2K
The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
8.2K

こちらも読む

関連記事

共著者、ジャーナル、引用グラフによってこの研究に関連する記事。

並び替え
Same author

Selective sensitivity of Ph-like B-cell acute lymphoblastic leukemia to BRG1 inhibition identifies a therapeutic vulnerability.

Leukemia·2026
Same author

FATP2-mediated lipid metabolism enhances chimeric antigen receptor T-cell therapy resistance in B-cell acute lymphoblastic leukemia.

Leukemia·2026
Same author

Multi-Omics Analysis Reveals Chronic Cisplatin Exposure Is Associated with Metabolic Rewiring Toward Glutathione Metabolism to Support Redox Adaptation in High-Grade Serous Ovarian Cancer.

Cancers·2026
Same author

Inhibition of ADSS2-mediated de novo AMP biosynthesis re-sensitizes acute myeloid leukemia to BH3 mimetics.

Nature cancer·2026
Same author

Targeting the METTL1/m7G axis as a therapeutic strategy in myeloid leukemia.

Blood·2026
Same author

An encyclopedic regulatory and functional atlas of RNA interactomes.

Nature methods·2026

関連する実験動画

Updated: Dec 14, 2025

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production
08:22

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Published on: May 31, 2020

5.4K

異なる経路からのシグナル入力で,B細胞変換が逆転する.

Lai N Chan1, Mark A Murakami2,3, Mark E Robinson1

  • 1Department of Systems Biology, City of Hope Comprehensive Cancer Center, Monrovia, CA, USA.

Nature
|July 24, 2020
PubMed
まとめ
この要約は機械生成です。

癌は変異が単一の腫瘍発生経路に 収束したときに発生します 単独では発生しません 抑制された経路を再活性化することで 変異を逆転させ,白血病の治療を強化できます

さらに関連する動画

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
07:12

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Published on: April 16, 2015

53.9K
Recombinant Retroviral Production and Infection of B Cells
09:19

Recombinant Retroviral Production and Infection of B Cells

Published on: February 18, 2011

14.5K

関連する実験動画

Last Updated: Dec 14, 2025

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production
08:22

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Published on: May 31, 2020

5.4K
Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
07:12

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Published on: April 16, 2015

53.9K
Recombinant Retroviral Production and Infection of B Cells
09:19

Recombinant Retroviral Production and Infection of B Cells

Published on: February 18, 2011

14.5K

科学分野:

  • 腫瘍学
  • 分子生物学
  • 遺伝学

背景:

  • 癌は遺伝子の突然変異によって発生します
  • 細胞の変容を誘導する特定の腫瘍学的経路が含まれる.
  • B細胞急性リンパ性白血病 (B-ALL) は,独特の遺伝的病変によって特徴付けられています.

研究 の 目的:

  • B-ALLにおける腫瘍学的経路の収束の役割を調査する.
  • 異なる経路が白血病発生にどのように影響するか理解するためです
  • B-ALLにおける腫瘍性経路を標的とした治療戦略を探求する.

主な方法:

  • 患者から採取した1148個のB-ALLサンプルを分析した.
  • 単細胞変異とフォスフォタンパク質の分析
  • STAT5とERKのシグナル伝達経路とその関連転写因子 (MYC,BCL6) を調査する.

主要な成果:

  • 白血病の発達には,細胞の分化段階の特徴である単一の腫瘍性経路の収束が必要です.
  • STAT5 (プロB細胞段階) やERK (プレB細胞段階) を活性化する変異は一般的だが,通常は競合するクローンに分離される.
  • 抑制された分岐経路の再活性化により 変換は逆転し 削除は加速した.

結論:

  • 主要な腫瘍発生因子の収束は白血病の発症に不可欠です.
  • 異なる信号経路は 変換の障壁となります
  • 抑制された分岐経路を再活性化することで,B-ALLの治療応答を向上させる新しい治療戦略が提供され,主な腫瘍原因の抑制と連携します.