生物化学和生物物理学档案在生物化学和生物物理学的发展领域发表高质量的原创文章和评论。研究领域包括：• 酶和蛋白质的结构、功能、调控。折叠、周转和翻译后加工• 生物氧化、自由基反应、氧化还原信号、加氧酶、P450 反应• 信号转导、受体、膜转运、细胞内信号。细胞和综合代谢。

The Archives of Biochemistry and Biophysics is a journal dedicated to the fields of biochemistry and biophysics, publishing high-quality original research articles and reviews. The areas of research include: the structure, function, and regulation of enzymes and proteins; folding, turnover, and post-translational modifications; biological oxidation, free radical reactions, redox signaling, oxygenases, and P450 reactions; signal transduction, receptors, membrane transport, and intracellular signaling; as well as cellular and integrated metabolism.

《Archives of Biochemistry and Biophysics》是一个专注于生物化学和生物物理学领域的期刊，发表高质量的原创研究文章和评论。研究领域包括：酶和蛋白质的结构、功能及调控；折叠、周转和翻译后加工；生物氧化、自由基反应、氧化还原信号、加氧酶及P450反应；信号转导、受体、膜转运和细胞内信号；细胞及综合代谢。

Archives of Biochemistry and Biophysics

Low levels of all of the enzymes required for urea synthesis via the urea cycle, including mitochondrial glutamine- and acetylglutamate-dependent carbamoyl-phosphate synthetase III (CPSase III) and cytosolic glutamine synthetase, are known to be present in liver of the teleost fish largemouth bass (Micropterus salmoides). The levels of these enzymes are higher than those in most other teleosts, but they are significantly lower than the levels present in liver of ureoosmotic elasmobranchs. The purpose of this study was to assess the physiological role of CPSase III in the context of urea synthesis in adult bass. The results showed that urea-N accounts for about 30% of the total nitrogen (ammonia-N plus urea-N) excreted under control conditions. The rate of urea-N excretion did not increase in response to exposure to 1 mM NH4Cl (3 days) or 0.25 mM NH4Cl (12 days) in the external water, except for a transient increase after a day or two of exposure. CPSase III activity in liver also did not increase in response to exposure to ammonia. Adult largemouth bass, while apparently ureogenic, are primarily ammonotelic and remain so even in the presence of relatively high concentrations of ammonia in the external environment. The total units of CPSase III activity in liver are not sufficient to account for the quantity of urea that is excreted. However, CPSase III and ornithine carbamoyltransferase (OCTase) activities were found to be present in intestinal tissue and, unexpectedly, in muscle tissue. The total units of CPSase III and OCTase in muscle, intestine, and liver appear to be sufficient to account for the observed rate of urea excretion. The sequence of CPSase III cDNA was determined, which permitted the use of ribonuclease protection assays to demonstrate the presence of CPSase III mRNA in these tissues.

Haiyan Kong

Dale D. Edberg

Joseph J. Korte

Wilmar L. Salo

Patricia A. Wright

Paul M. Anderson

Nitrogen Excretion and Expression of Carbamoyl-phosphate Synthetase III Activity and mRNA in Extrahepatic Tissues of Largemouth Bass (Micropterus salmoides)

Mechanical environments were associated with alterations in bone metabolism. Ion channels present on bone cells are indispensable for bone metabolism and can be directly or indirectly activated by mechanical stimulation. This review aimed to discuss the literature reporting the mechanical regulatory effects of ion channels on bone cells and bone tissue. An electronic search was conducted in PubMed, Embase and Web of Science. Studies about mechanically induced alteration of bone cells and bone tissue by ion channels were included. Ion channels including TRP family channels, Ca2+ release-activated Ca2+ channels (CRACs), Piezo1/2 channels, purinergic receptors, NMDA receptors, voltage-sensitive calcium channels (VSCCs), TREK2 potassium channels, calcium- and voltage-dependent big conductance potassium (BKCa) channels, small conductance, calcium-activated potassium (SKCa) channels and epithelial sodium channels (ENaCs) present on bone cells and bone tissue participate in the mechanical regulation of bone development in addition to contributing to direct or indirect mechanotransduction such as altered membrane potential and ionic flux. Physiological (beneficial) mechanical stimulation could induce the anabolism of bone cells and bone tissue through ion channels, but abnormal (harmful) mechanical stimulation could also induce the catabolism of bone cells and bone tissue through ion channels. Functional expression of ion channels is vital for the mechanotransduction of bone cells. Mechanical activation (opening) of ion channels triggers ion influx and induces the activation of intracellular modulators that can influence bone metabolism. Therefore, mechanosensitive ion channels provide new insights into therapeutic targets for the treatment of bone-related diseases such as osteopenia and aseptic implant loosening.

Kun Zhang

Xuening Liu

Lifu Wang

Zhongcheng Liu

Qiong Yi

Bin Geng

Xiangyi Chen

Dechen Yu

YaYi Xia

Archives of biochemistry and biophysics

Arch Biochem Biophys

The mechanosensory and mechanotransductive processes mediated by ion channels and the impact on bone metabolism: A systematic review.

Cervical cancer is one of the most common cancers in women worldwide. Hexokinase 2 (HK2) is responsible for phosphorylating glucose into glucose-6-phosphate, which is required for tumorigenesis and metastasis.

Chunyan Liu

Yangyang Li

Changyan Dong

Luyun Qu

Ying Zuo

E6E7 regulates the HK2 expression in cervical cancer via GSK3β/FTO signal.

In addition to ATP synthesis, mitochondria are highly dynamic organelles that modulate apoptosis, ferroptosis, and inflammasome activation. Through executing these varied functions, the mitochondria play critical roles in the development and progression of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Friedreich ataxia, among others. Impaired mitochondrial biogenesis and abnormal mitochondrial dynamics contribute to mitochondrial dysfunction in these diseases. Additionally, dysfunctional mitochondria play critical roles in signaling for both inflammasome activation and ferroptosis. Therapeutics are being developed to circumvent inflammasome activation and ferroptosis in dysfunctional mitochondria. Targeting these aspects of mitochondrial dysfunction may present viable therapeutic strategies for combatting the neurodegenerative diseases. This review aims to summarize the role of the mitochondria in the development and progression of neurodegenerative diseases and to present current therapeutic approaches that target mitochondrial dysfunction in these diseases.

Joseph Johnson

Elizabeth Mercado-Ayon

Yesica Mercado-Ayon

Yi Na Dong

Sarah Halawani

Lucie Ngaba

David R Lynch

Mitochondrial dysfunction in the development and progression of neurodegenerative diseases.

线粒体功能障碍在神经退行性疾病发生和进展中的作用。

Dihydrodipicolinate synthase (DHDPS) catalyzes the first step in the pathway for the biosynthesis of L-lysine in most bacteria and plants. The substrates for the enzyme are pyruvate and L-aspartate-β-semialdehyde (ASA). The product of the reaction was originally proposed to be 2,3-dihydrodipicolinate (DHDP), but has now generally been assumed to be (4S)-4-hydroxy-2,3,4,5-tetrahydro-(2S)-dipicolinate (HTPA). ASA is unstable at high pH and it is proposed that ASA reacts with itself. At high pH ASA also reacts with Tris buffer and both reactions are largely reversible at low pH. It is proposed that the basic un-protonated form of the amine of Tris or the α-amine of ASA reacts with the aldehyde functional group of ASA to generate an imine product. Proton NMR spectra of ASA done at different pH values shows new NMR peaks at high pH, but not at low pH, confirming the presence of reaction products for ASA at high pH. The enzymatic product of the DHDPS reaction was examined at low pH by proton NMR starting with either 3 h-pyruvate or 3 d-pyruvate and identical NMR spectra were obtained with four new NMR peaks observed at 1.5, 2.3, 3.9 and 4.1 ppm in both cases. The NMR results were most consistent with DHDP as the reaction product. The UV-spectral studies of the DHDPS reaction shows the formation of an initial product with a broad spectral peak at 254 nM. The DHDPS reaction product was further examined by reduction of the enzymatic reaction components with borohydride followed by GC-MS analysis of the mixture. Three peaks were found at 88, 119 and 169 m/z, consistent with pyruvate, homoserine (reduction product of ASA), and the reduction product of DHDP (1,2,3,6-tetrahydropyridine-2,6-dicarboxylate). There was no indication for a peak associated with the reduced form of HTPA.

William E Karsten

Susan A Nimmo

Jianguo Liu

Lilian Chooback

Identification of 2, 3-dihydrodipicolinate as the product of the dihydrodipicolinate synthase reaction from Escherichia coli.

鉴定2,3-二氢二吡啶羧酸为大肠杆菌二氢二吡啶羧酸合成酶反应的产物。

Exosomes are membrane-bound extracellular vesicles that play a role in exchanging biological products across membranes and serve as intermediaries in intercellular communication to maintain normal homeostasis. Numerous molecules, including lipids, proteins, and nucleic acids are enclosed in exosomes. Exosomes are constantly released into the extracellular environment and exhibit distinct characteristics based on the secreted cells that produce them. Exosome-mediated cell-to-cell communication has reportedly been shown to affect multiple cancer hallmarks, such as immune response modulation, pre-metastatic niche formation, angiogenesis, stromal cell reprogramming, extracellular matrix architecture remodeling, or even drug resistance, and eventually the development and metastasis of cancer cells. Exosomes can be used as therapeutic targets and possible diagnostic biomarkers by selectively loading oncogenic molecules into them. We highlight the important roles that exosomes play in cancer development in this review, which may lead to the development of fresh approaches for future clinical uses.

Manasi S Pote

Rajesh N Gacche

Exosomal Signaling in Cancer Metastasis: Molecular Insights and Therapeutic Opportunities

癌症转移中的外泌体信号传导：分子见解与治疗机遇

Since their original proposal in 2008, a number of broadly distributed flavoprotein systems catalyzing electron bifurcation have been identified that play key roles in the bioenergetics of anaerobic bacteria and archaea. While the overall thermodynamics of flavin-based electron bifurcation are now quite well-understood, the same cannot be said of their kinetic behavior. The present account represents a summary of results obtained with several electron-electron bifurcating systems, shamelessly focusing on work done in the authors' laboratory.

Russ Hille

Dimitri Niks

Wayne Vigil

Jessica Tran

Steve Ortiz

Kevin Menjivar

Derek Nguyen

Kinetic studies of bifurcating flavoproteins

黄素蛋白分支动力学研究

Annexin A2 (ANXA2) is a Ca2+-dependent multifunctional protein containing five Ca2+-binding domains, but their functional significance and difference remain unclear. Herein, glutamic acid (E) or aspartic acid (D) in five Ca2+-binding domains of canine ANXA2 (98.82 % and 96.76-99.41 % identical to ANXA2 from human and other mammals, respectively) was substituted by alanine (A) using site-directed mutagenesis. Recombinant ANXA2 wild-type (WT) and E53A, E96A, D162A, E247A and D322A mutants were constructed and expressed using a bacterial expression system followed by high-affinity purification using nickel-nitrilotriacetic acid (Ni-NTA) matrix. Efficacies of their expression and purification were confirmed by SDS-PAGE and Western blotting. Their amino acid sequences were verified by nanoLC-ESI-Qq-TOF tandem mass spectrometry. ATR-FTIR spectroscopy revealed that their secondary structure significantly differed (α-helix decreased but random coil increased in all mutants). Analyses of physicochemical properties revealed that molecular weight slightly decreased, whereas isoelectric point, aliphatic index, grand average of hydropathicity, electrostatic potential and molecular hydrophobicity potential slightly increased in all the mutants compared with WT. Interestingly, Ca2+-binding capability of these mutants (particularly E96A and D322A) significantly decreased from that of WT. In summary, secondary structure, physicochemical properties, and Ca2+-binding capability of E53A, E96A, D162A, E247A and D322A mutants of ANXA2 significantly differed from its WT, consistent with the loss of negatively charged E/D. In particular, E96A and D322A exhibited the lowest Ca2+-binding capability. These data and recombinant proteins would be useful for further investigations of the Ca2+-dependent functions of individual Ca2+-binding domains in ANXA2.

Sunisa Yoodee

Sirikanya Plumworasawat

Thanyalak Malaitad

Paleerath Peerapen

Visith Thongboonkerd

Differential structural characteristics, physicochemical properties, and calcium-binding capabilities of annexin A2 wild-type versus E53A, E96A, D162A, E247A and D322A mutants

 annexin A2野生型与E53A、E96A、D162A、E247A和D322A突变体的结构特征、理化性质及钙结合能力的差异

Silica shell is considered to be a promising design that enhances nanocomposite stability, cellular internalization, and consequentially therapeutic impacts by overcoming their aggregation under physiological conditions. This study addressed synthesizing silica-layered iron oxide-based nanoparticles (SCINPs) with different shell thicknesses (1-SCINPs, 2-SCINPs, 3-SCINPs, and 4-SCINPs). Also, the impact of shell thickness on the nanoparticle's cellular internalization and the radio-sensitizing effect of prepared nano-formulations were assessed. The physical properties of the synthesized nanoparticles were examined using transmission electron microscopy (TEM), atomic force microscopy (AFM), dynamic light scattering (DLS), vibrating sample magnetometry (VSM), and X-ray diffraction (XRD). Cytotoxicity assay, oxidative stress parameters, and comet assay were used to investigate the radio-sensitizing effect of various nanoformulations. Results revealed that the mean diameter of prepared oxide-based nanoparticles (INPs) was about 12.63 ± 1.36 nm, and the shell thickness for 1-SCINPs, 2-SCINPs, 3-SCINPs, and 4-SCINPs was 22.58 ± 3.51, 26.13 ± 1.40, 46.95 ± 3.10 and 60.30 ± 4.30 nm, respectively. Interestingly, we found that in cells treated with 40 μg/ml of INPs, their viability decreased to 44.6 %. Meanwhile, the viability was 41.69 % and 39.4 % for cells treated with 1-SCINPs and 2-SCINPs, respectively. This means that a thicker silica shell led to a decreased impact on radiosensitization. This was attributed to the influence of surface properties and size of SCINPs on their cellular uptake and the secondary electrons' entrapment within thicker shells upon radiation exposure. Cell viability test, comet assay and oxidative stress parameters show that 2-SCINPs formulations had the most potent radiosensitizing effect (with the highest dose enhancement factor equal to 2.1) when combined with radio-treatment. The results suggest that optimizing the silica shell thickness is critical for maximizing the therapeutic efficacy of SCINPs, with 2-SCINPs showing the highest radiosensitization effect.

Mohamed M Fathy

Omnia A Saad

Heba M Fahmy

Radiosensitization impact assessment of silica-layered iron oxide nanocomposites with various shell thickness

二氧化硅-层状氧化铁纳米复合材料在不同壳层厚度下的放射增敏效应评估

Ca2+/calmodulin-dependent protein kinase II α (CaMKIIα) "autonomous" activation induced by Thr286 phosphorylation has a crucial role in synaptic plasticity. Previous studies showed that in Alzheimer's disease brain, CaMKIIα autophosphorylation at Thr286 is reduced while the level of cysteine-oxidized CAMKIIα is elevated. We performed tryptic mapping of the oxidized CaMKIIα and discovered the formation of a disulfide between the N-terminal Cys6 and the regulatory domain Cys280. The apparent pKa values of Cys6 and Cys280 are 7.1 and 7.7, respectively, lower than the 8.5 for free Cys. The low apparent pKa of Cys6 facilitates the oxidation of its thiol to the sulfenic acid at physiological pH. The thiolate of Cys280 can then attack the sulfenic acid to form a disulfide. Using an antibody against phosphorylated Thr286, we showed that disulfide formation prevents Thr286 phosphorylation. CaMKIIα autonomous activation induced by disulfide formation is much lower than the autonomous activation induced by phosphorylation. The decreased autonomous activation may contribute to the synaptic impairment of Alzheimer's disease. We also generated a CaMKIIα mutant in which Cys6 was mutated to Ser6. This mutation prevented disulfide formation and restored autonomous activation induced by phosphorylation. Our findings provide insight into the mechanistic details of CaMKIIα autonomous activation induced by disulfide formation that may contribute to the impairment of long-term potentiation in Alzheimer's disease.

Nathália Rocco-Machado

Max Deng

Yi He

Rodney L Levine

Oxidation of CaMKIIα cysteines inhibits autonomous activation induced by phosphorylation

CaMKIIα半胱氨酸氧化抑制磷酸化诱导的自主激活

Abbreviation	Arch. Biochem. Biophys.
Journal Impact	3.70
Quartiles(Global)	BIOPHYSICS(Q1)

ISSN	0003-9861, 1096-0384
h-index	194

Publication Information	Publisher: Academic Press Inc.，Publishing cycle: Semimonthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1951，Proportion of original research papers: 92.93%，Self Citation Rate:2.60%， Gold OA Rate: 19.97%
Average review cycle	网友分享经验：平均1月来源Elsevier官网：平均6.3周
Average recruitment ratio	网友分享经验：约25%

Archives of Biochemistry and Biophysics

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